ArticlePDF Available

The Role of Early Experience in Shaping Behavioral and Brain Development and Its Implications for Social Policy



This article provides a targeted review of the scientific literature on the effects of experience on early brain and behavioral development and later outcome as it pertains to risk for some forms of child psychopathology. It is argued that ample evidence exists indicating that the prenatal and early postnatal years likely represent a sensitive period with respect to the effects of stress on the developing nervous system and behavioral outcome, and with respect to the long-term beneficial effects of early interventions on brain and behavioral development for some genetically based disorders, such as phenylketonuria and autism. Moreover, evidence suggests that parental mental health during the first years of life has a significant influence on early brain activity and behavior, and long-term behavioral outcome. It is concluded that, although prevention and early intervention efforts should not exclusively focus on the earliest years of development, such efforts should begin during this period. By directing such efforts toward promoting optimal prenatal and infant-toddler development, the long-term negative consequences of factors that have their greatest influences during early development and which set the stage for future development can be minimized or avoided entirely. Several recommendations for public policy and future research pertaining to the effects of early experience on child outcome are offered.
Development and Psychopathology, 12 (2000), 695712
Copyright 2000 Cambridge University Press
Printed in the United States of America
The role of early experience in shaping
behavioral and brain development and its
implications for social policy
University of Washington
This article provides a targeted review of the scientific literature on the effects of experience on early brain and
behavioral development and later outcome as it pertains to risk for some forms of child psychopathology. It is
argued that ample evidence exists indicating that the prenatal and early postnatal years likely represent a sensitive
period with respect to the effects of stress on the developing nervous system and behavioral outcome, and with
respect to the long-term beneficial effects of early interventions on brain and behavioral development for some
genetically based disorders, such as phenylketonuria and autism. Moreover, evidence suggests that parental mental
health during the first years of life has a significant influence on early brain activity and behavior, and long-term
behavioral outcome. It is concluded that, although prevention and early intervention efforts should not exclusively
focus on the earliest years of development, such efforts should begin during this period. By directing such efforts
toward promoting optimal prenatal and infanttoddler development, the long-term negative consequences of factors
that have their greatest influences during early development and which set the stage for future development can be
minimized or avoided entirely. Several recommendations for public policy and future research pertaining to the
effects of early experience on child outcome are offered.
from birth to 3 years; the Family and Medical
Leave Act enacted in 1993, which recognized
In the past few decades, efforts at promoting
optimal development in children have increas-
ingly focused on the earliest years of life, the importance of parents spending time with
their young infants after birth before returningincluding the prenatal period, infancy, and
toddlerhood. Broad-based policy changes re- to work; and Early Head Start created in
1994, which provided education and childcareflecting a focus on early development have
included PL 99-457 enacted in 1986, which to at-risk children from birth to 3 years. The
rationale behind these efforts has been basedprovided services to handicapped children
largely on an increased understanding of nor-
mal infant behavior and development and of
The writing of this article and the research on the effects the negative influences of factors such as poor
of maternal depression on infant brain activity reported
nutrition, drug exposure, abuse and neglect,
herein were supported by grants from the National Insti-
and parent psychopathology and stress on
tute of Mental Health (MH47117) and the National Insti-
early development and later outcome (Nelson,
tutes of Child Health and Human Development, and
in press).
Deafness and Communication Disorders (POIHD34565).
Lara Embry, Karin Frey, Lili Lengua, Charles Nelson, The idea that early experience is important
and Joanna Self provided helpful critiques of early ver-
for promoting optimal long-term outcomes for
sions of this paper.
children has been supported by studies of be-
Address correspondence and reprint requests to: G.
havioral outcomes and early intervention in
Dawson, Department of Psychology and Center on Hu-
various at-risk and developmentally disabled
man Development and Disability, Box 357920, Univer-
sity of Washington, Seattle, WA 98195. populations. Examples of such research in-
G. Dawson, S. B. Ashman, and L. J. Carver696
clude studies of (a) the effects of prenatal nu- tion discussed the importance of the new
brain science for understanding children’s de-trition and exposure to toxic substances on
brain and behavioral development (Morgan & velopment and for public policy. As a result,
leaders in several states enacted policyGibson, 1991; Sonderegger, 1992; Spohr,
Williams, & Steinhausen, 1993); (b) the ef- changes based on what they viewed as the
new research on brain development. Numer-fects of maternal depression during pregnancy
and infancy on later cognitive and emotional ous policy initiatives and exploratory panels
emerged to address the issue of early experi-functioning in children (Goodman & Gotlib,
1999); and (c) the effects of early interven- ence and brain development in several states
(Groginsky, Christian, & McConnell, 1998).tions for improving cognitive, social, and aca-
demic functioning in children from economi- In 1997, the Federal Early Childhood Devel-
opment Act was introduced, stressing the im-cally and socially disadvantaged backgrounds
(Campbell & Ramey, 1994) and in children portance of early experience on brain devel-
opment and outcome for children.with genetic disorders that affect brain devel-
opment, such as autism and phenylketonuria The recent public and political enthusiasm
over the effects of early environment on brain(PKU; Dawson & Osterling, 1997; Wappner,
Cho, Kronmal, Schuett, & Seashore, 1999). development subsequently led to a backlash
among some scientists who were concernedAt the same time that research and policy
have increasingly stressed the importance of that the public and policymakers have over-
simplified a complex issue. In fact, the publicearly experience in the development of chil-
dren, new techniques for studying infant be- hype over the implications of brain science
and the resulting recent critiques and contro-havior and brain activity have been devel-
oped, allowing developmental scientists to versy may have had the unfortunate effect of
a waning of interest in early childhood, withbegin to learn more about relations between
biology and behavior in infants and children a loss of policies with the potential to benefit
children (Thompson & Nelson, in press).(reviewed in Dawson & Fischer, 1994). In the
1990s, as these intriguing studies were pub- Nevertheless, scientists such as Bruer (1999),
Greenough (1997), and others have raised im-lished and discussed in the popular media,
public interest in early brain development and portant questions regarding what is actually
known about the effects of early experiencebehavior began to swell. The effects of early
experience on the developing brain, in partic- on brain development. In his recent book,
Bruer (1999) argues that the media have beenular, became of interest after a White House
conference on the topic was held in the spring misguided in promoting the myth that the first
3 years of a baby’s life can determine aof 1997. The White House conference coin-
cided with a national media campaign focused child’s long-range outcome. He further de-
scribes what he refers to as “three neuroscien-on early development, which included broad-
casts on “Good Morning America” and fea- tific strands” that taken together form the
“myth of the first three years.” In this article,ture articles in Newsweek. Concurrently, pub-
lic policy documents on the relation between we will discuss each of these strands and what
can be scientifically concluded about their im-brain science and early development were
published by major foundations interested in portance for understanding the effects of early
experience on later outcome. We will coverpromoting the health and welfare of children,
including Starting Points, published by the in some detail what is known about the devel-
opment and underlying mechanisms involvedCarnegie Corporation, and Rethinking the
Brain: New Insights Into Early Development, in synaptic formation and efficiency. We will,
in addition, describe the growing body of evi-published in conjunction with the White
House conference. These documents were dence demonstrating that exposure to early
maladaptive experiences, such as prenatal andcovered in the popular media and read by pol-
icymakers and politicians interested in public postnatal stress and parental psychopathology,
does indeed have long-term implications forhealth and child development. Keynote speak-
ers at the 1997 National Governor’s Associa- brain and behavioral development. The impli-
Role of experience 697
cations of the research pertaining to the ef- aptic formation and pruning and behavioral
development. First, it is known that some dis-fects of early experience on brain and behav-
ior for public policy will be considered in the orders that involve mental retardation, such as
Fragile X, are associated with abnormal syn-concluding section of this paper.
aptic pruning, specifically with excess syn-
Synaptogenesis and the Remarkable
apses (Comery, Harris, Willems, Oostra, Ir-
Period of Early Brain Growth
win, Weiler, & Greenough, 1997). While
these disorders are caused by genetic abnor-The first neuroscientific strand that Bruer de-
scribes pertains to the fact that the brain de- malities rather than faulty early experiences,
it is noteworthy that there does appear to be avelops rapidly during the prenatal and early
postnatal months. Remarkably, early in a relation between synaptic density and intelli-
gence, with higher numbers of synapses asso-child’s life the brain produces trillions more
synapses than are found in adulthood. During ciated with lower intelligence.
Second, it appears that increased early en-the first 3 years of life, synapses form at a
phenomenal rate. In humans, it appears that vironmental stimulation does not necessarily
lead to increases in synaptic formation duringrapid synapse formation begins during the
first few postnatal months and reaches highest the period of rapid synaptic proliferation and
pruning, at least for the visual system in non-densities at about 3 months for sensory cortex
and about 23.5 years for frontal cortex (Hut- human primates (Bourgeois, Jastreboff, &
Rakic, 1989). It is clear, however, that experi-tenlocher, 1994; Huttenlocher & Dabholkar,
1997; Rakic, Bourgeois, & GoldmanRakic, ence in some instances can alter the synaptic
formation and organization in the cortex (see1994). Furthermore, this period of peak syn-
aptic density coincides in time with the emer- Kolb, Forgie, Gibb, Gorny, & Rowntree,
1998, for a review of this rich set of data).gence of important cognitive skills, including
early manifestations of working memory (Di- Animals raised in complex, enriched environ-
ments have more synapses in certain parts ofamond & GoldmanRakic, 1989). For exam-
ple, a study by Bell and Fox (1994) showed their brains compared to animals raised in
nonenriched environments (Greenough, Black,that infants who are able to achieve early
frontal tasks involving working memory dis- & Wallace, 1987). Furthermore, changes in
synaptic organization as a result of experienceplayed increased electrical brain activity over
the frontal scalp region. Put simply, neurosci- are correlated with changes in behavioral per-
formance in both animals and humans (Kolbence and developmental science have shown
that early life is a time of truly remarkable et al., 1998). For example, Jacobs and
Scheibel (1993) and Jacobs, Schall, andgrowth in terms of both brain and behavior.
However, as Bruer points out, there is still rel- Scheibel (1993) reported a relation between
extent of dendritic arborization (which wouldatively little known about how early experi-
ences, such as parenting, actually affect brain act to increase the number of synapses) and
the amount of education received. Interest-development, such as the rate or patterns of
synaptic formation and pruning, or even about ingly, research has shown that the effect of
enriched experience on synaptic number andthe relation between changes in regional syn-
aptic densities and specific cognitive skills organization is highly dependent upon the
age. Enriched experience during early postna-(e.g., peak synaptic densities in the frontal re-
gion and the emergence of early frontal lobe tal life appears to lead to a decrease in spine
density on the neuron but to have no effect onskills). Although it is intriguing that certain
biological events such as rapid synaptic pro- dendritic length (Kolb et al., 1998).
Science is still addressing the question ofliferation and the emergence of certain cogni-
tive skills co-occur in development, such a co- precisely how experiences affect the pattern
of selective elimination and responsiveness ofoccurrence does not prove that there is any
causal relation between these two processes. neural networks formed during early develop-
ment, as opposed to the sheer quantity of syn-There are, however, several things that are
known about the relation between early syn- apses, which appears, in large part, to be
G. Dawson, S. B. Ashman, and L. J. Carver698
under genetic control. It is known that experi- ute to memory. A recent report described the
formation of new dendritic spines followingence can and does play a role in selecting and
establishing preferentially active synapses. LTP (Toni, Buchs, Nikonenko, Bron, & Mul-
ler, 1999). This morphological synapticSelective amplification of specific neural
groups occurs via a competitive process as a change may also lead to changes in synapse
responsiveness.result of the frequency and intensity of stimu-
lation (Edelman, 1987; Hebb, 1949). Once a Consistent with the idea that LTP underlies
the formation of memories, a number of stud-specific pattern of neuronal groups is selected
in a mapped area, exposure to the same or ies have shown that blocking LTP through re-
ceptor antagonists or genetic manipulationssimilar stimuli is likely to preferentially acti-
vate previously selected neuronal groups. In leads to impaired memory performance in ex-
perimental animals (Lu, Jia, Janus, Hender-this way, it is hypothesized, developing neural
patterns become stabilized and less suscepti- son, Gerlai, Wojtowicz, & Roder, 1997; May-
ford, Bach, Huang, Wang, Hawkins, &ble to change over time (Edelman, 1989).
Such maps are believed to involve cortical Kandel, 1996). In addition, enhancing LTP by
manipulating second-messenger cascades in-sensory and motor maps as well as the brain
regions with which these cortical areas inter- volved in LTP is correlated with improved
memory performance (Barad, Bourtchou-act, such as limbic regions. Research is shed-
ding light on the mechanisms involved in se- ladze, Winder, Golan, & Kandel, 1998). In
addition to memory formation, some researchlecting and establishing preferentially active
neural patterns. Repeated and synchronous ac- suggests that components of LTP that are in-
volved in gene regulation are important fortivation of neighboring neurons strengthens
the connections between them, and allows consolidation of memory traces (Bourtchou-
ladze, Frenguelli, Blendy, Cioffi, Schutz, &them to fire more efficiently.
Decades ago, Hebb (1949) suggested that Silva, 1994). Thus, although there are some
reports that eliminating or decreasing LTPeither morphological or metabolic changes
might underlie changes in synaptic efficiency. does not affect memory (Meiri, Sun, Segal, &
Alkon, 1998), most research suggests thatMuch attention has been focused on long-
term potentiation (LTP), which may be a met- they are related.
Although it is becoming increasingly clearabolic mechanism for memory formation
(Chen & Tonegawa, 1997; Malenka & Nicoll, that LTP is likely involved in memory forma-
tion, there are a number of aspects of the1999). In LTP, high-frequency activation of
glutamate receptors results in a long-lasting physiological basis of memory that still must
be understood. LTP is most frequently studiedstrengthening of the synaptic connection such
that for intervals of up to hours the synapse in the hippocampus, a structure thought to be
involved in the formation of memory tracesresponds more readily and efficiently to acti-
vation. In LTP, non-N-methyl-
-aspartate (Chen & Tonegawa, 1997; Malenka & Nicoll,
1999). It has yet to be determined, however,(NMDA) glutamate receptors are activated,
depolarizing the postsynaptic membrane and how memory traces are stored in long-term
memory and what role, if any, synaptic plas-allowing for activation of NMDA glutamate
receptors. Most likely, both postsynaptic and ticity plays in the storage process. There is
some suggestion that, in addition to memory,presynaptic mechanisms are involved in this
process. Removal of the magnesium block LTP may be involved in activity-dependent
formation of neural circuitry, certainly in sen-that typically prevents activation of the
NMDA receptor allows calcium to enter the sory systems (Chen & Tonegawa, 1997;
Katz & Shatz, 1996). One hypothesis yet topostsynaptic cell, beginning a cascade of sec-
ond-messenger events that ultimately leads to be tested is that experience-dependent mecha-
nisms such as LTP might also be involved inlong-lasting changes in synaptic strength. In
addition to the metabolic changes that are in- building associative networks that form the
basis for memories as well.volved in LTP, structural changes have been
identified and such changes may also contrib- In summary, ample scientific evidence in-
Role of experience 699
dicates that experiences can influence the for- development, such as PKU and autism, have
shown that optimal long-term outcome inmation, strength, and efficiency of synapses.
Research is revealing the mechanisms in- terms of IQ and adaptive behavior critically
depends on intervention during the early yearsvolved in experience-dependent changes in
synaptic efficiency. However, it is unknown of life. For PKU, intervention must begin
when the infant is less than 21 days old (Wap-to what extent the early years of life, because
of the tremendous changes in the sheer num- pner et al., 1999). It has been demonstrated
that children with autism who receive inten-ber of synapses that take place during this
time, represent a particularly sensitive period sive interventions by 23 years of age fare
substantially better than those who receive in-for selecting and establishing preferentially
active patterns of neural networks that are less tervention after this age (see Dawson & Os-
terling, 1997, for review of early interventionsusceptible to change later in life.
studies in autism). Moreover, recent research
has shown that relatively common variations
Sensitive Periods and Long-Term
in early experience related to stress and mal-
Effect of Early Experience
adaptive parenting can have long-term effects
on development. In the next sections, we willThis brings us to the second and third neuros-
cientific strands that, according to Bruer, form review in detail what is known about the in-
fluences of early stress and maternal depres-the “myth of the first three years.” These per-
tain to the related notions that (a) the early sion on development. It will be concluded that
early stress and maternal depression representyears of development represent a sensitive pe-
riod for brain and behavioral development and relatively common deviations in early experi-
ence that appear to negatively influence both(b) early experiences can have long-term in-
fluences on brain and behavioral develop- brain and behavioral development.
ment. To begin, it is known that there are sen-
sitive periods in brain development (Knudsen,
Effects of early stress
1999); that is, there are periods in develop-
ment during which specific types of experi- Numerous studies, most involving animals
but some in humans, have documented theence are needed for the brain to develop
normally. The term “experience-expectant” de- negative effects of early exposure to stress
and social deprivation on both brain and be-velopment has been used to refer to develop-
mental processes that involve a readiness of the havioral development, and on long-term out-
come. Prenatal stress, for example, has beenbrain to receive specific types of information
from the environment (Greenough et al., 1987). shown to have numerous and varied effects
on the subsequent development of offspring.This readiness occurs during sensitive periods
in which specific types of information are reli- The function of the hypothalamicpituitary
adrenal (HPA) axis, the major hormonal stressably present for most members of the species.
This information can be visual, social, affec- response system, is affected in the offspring
of rats exposed to high levels of stress hor-tive, and cognitive. It has been argued that the
overproliferation of synapses during early post- mones either by injection or by exposure to
stress-inducing events (e.g., handling, re-natal life reflects the brain’s readiness to re-
ceive expected information during this period, straint, light, heat, cold). Offspring of preg-
nant rats injected with adrenocorticotropinwith the subset of synapses being selectively
retained depending on experience (Black, hormone (ACTH) showed increased basal
levels of corticosterone and decreased levelsJones, Nelson, & Greenough, 1998).
Studies have clearly demonstrated sensi- in response to stress (Fameli, Kitraki, & Styli-
anopoulou, 1994). In these offspring, the HPAtive periods for the development of language
and visual systems (Levay, Wiesel, & Hubel, system was hyperaroused during baseline
conditions and was overwhelmed and unable1980; Newport, 1990). Also, studies of chil-
dren at risk for cognitive and social impair- to respond during stressful conditions. This
result suggests that the systems that typicallyment due to genetic disorders that affect brain
G. Dawson, S. B. Ashman, and L. J. Carver700
regulate the activity of the HPA system do not prenatal stress on regulation of the HPA axis
and on brain development seem to be strongerfunction normally in cases of prenatal stress.
The HPA axis is regulated by a complex sys- for females than for males (e.g., Fride &
Weinstock, 1989; Kinsley, Mann, & Bridges,tem involving Type I glucocorticoid receptors
in the hippocampus and Type II receptors 1989). The maternal behavior of rats that were
themselves stressed prenatally clearly differsthroughout the brain (Weinstock, 1997). Dis-
regulation of this feedback system can lead to from that of nonprenatally stressed dams
(Weinstock, Fride, & Hertzberg, 1988). Thisincreased response to stressors, as well as an
inability to adapt to ongoing stress (Wein- raises the interesting possibility of multigen-
erational effects of prenatal stress, an issuestock, 1997).
In nonhuman primates, prenatal stress is that has yet to be well examined in the litera-
ture. In summary, there is evidence to suggestassociated with increased basal levels of
ACTH in plasma, as well as increased ACTH that prenatal stress results in long-term
changes in both brain and behavior in ani-levels in response to stress situations of vary-
ing degree in the offspring (Clarke, Wittwer, mals.
In comparison to the animal literature, lessAbbott, & Schneider, 1994). Behavioral ef-
fects have also been reported in infant mon- is known about the effects of prenatal stress
in humans. The majority of research in thekeys born to mothers that were stressed dur-
ing pregnancy. Monkeys that were exposed to area is retrospective, such as studies in which
parents respond to questionnaires about theirrepeated unpredictable noise in a darkened
room gave birth to infants that exhibited in- pregnancy history (Lobel, 1994). Children
whose mothers’ were exposed to a variety ofcreased behaviors associated with disturbance
(clinging to another monkey, clinging to an stressors during pregnancy were found to
have less optimal outcomes, including emo-artificial surrogate monkey, or self-directed
motor activity) and decreased motor and ex- tion regulation problems and motor delays
(Meier, 1985; Stott, 1973). The prospectiveploratory behaviors (locomotion, play, explo-
ration of the environment, and climbing) com- studies that have been done have primarily fo-
cused on very basic indicators of health andpared to infant monkeys born to nonstressed
mothers (Schneider, 1992a). Changes in cog- brain development such as birth weight, head
size, and risk for prematurity. Although thesenitive ability have also been noted in prena-
tally stressed rats and monkeys. In rats, per- are likely important factors in the future cog-
nitive and social development of the child,formance on a delayed alteration task was
impaired in the offspring of females exposed there is little direct evidence from studies in-
vestigating outcomes in children exposed toto the presence of a cat during the gestational
period (Lordi, Protais, Mellier, & Caston, stress in prenatal or early life. Indirect links
between head size and HPA responsiveness1997). In prenatally stressed rhesus monkeys,
the development of object permanence was (Ramsay & Lewis, 1995) suggest that prenatal
stress may be related to later HPA responsive-delayed compared to controls (Schneider,
1992b). ness (Glover, 1997), but the relation between
stress and head size is not made directly inThe mechanism responsible for these be-
havioral changes may lie in brain develop- the Ramsay and Lewis study. Thus, a relation
between stress response and prenatal stress inment changes that occur as a result of prenatal
stress. In rats exposed to prenatal stress, mild the human is hypothetical at best: infants pre-
natally exposed to stress have small heads,stressors resulted in an increase in acetylcho-
line in the hippocampus (Day, Koehl, De- and infants with small heads have abnormal
stress responses. Direct measures of the activ-roche, Le Moal, & Maccari, 1998). In addi-
tion, decreases in levels of dopamine and ity of the HPA axis are required to determine
precisely the effects on the system of prenatalincreases in levels of serotonin were discov-
ered in the brains of adult rats exposed to stress in the developing human before it can
concluded that results are truly parallel tostress hormones prenatally (Fameli et al.,
1994). those found in nonhuman primates and rats.
Studies of animals and humans also haveInterestingly, in many studies the effects of
Role of experience 701
demonstrated that early social deprivation and tions as well as changes in CRF neural sys-
tems. Similarly, Plotsky and Meaney (1993)exposure to high levels of stress during the
early postnatal period are related to poor so- found that maternal separation during the first
2 weeks of life resulted in elevated stress re-cial outcomes and alterations in psychobio-
logical functioning. Exposure to stress during sponses in adult rats.
Studies of nonhuman primates have dem-the postnatal period is associated with in-
creased levels of glucocorticoids, and gluco- onstrated similar long-term consequences of
early life stress (Capitanio, Rasmussen, Sny-corticoids have been shown to have harmful
effects on the developing brain. Evidence now der, Laudenslager, & Reite, 1986; Coplan,
Andrews, Rosenblum, Owens, Friedman,indicates that maternal behavior is important
for regulation of the stress response. In rats, Gorman, & Nemeroff, 1996). Coplan et al.
(1996) exposed bonnet macaques to eithermaternal separation stimulates HPA axis
activity and leads to elevated corticosterone predictable or unpredictable rearing condi-
tions by varying the amount and predictabilitylevels, as well as changes in, corticotropin re-
leasing factor (CRF) concentrations and re- of foraging that mothers needed to do to ac-
quire food. Years later, compared to primatesceptor number (Kuhn, Pauk, & Schanberg,
1990; Kuhn & Schanberg, 1998; Pihoker, exposed to predictable high foraging or pre-
dictable low foraging conditions, primatesOwens, Kuhn, Schanberg, & Nemeroff,
1993). Maternal behaviors, such as feeding exposed to variable foraging conditions ex-
hibited elevated cerebrospinal fluid concentra-and stroking, can weaken this adrenocortical
response to maternal separation. Suchecki, tions of CRF. Capitanio et al. (1986) reported
that monkeys who had experienced maternalRosenfeld, and Levine (1993) have shown
that, in maternally deprived rat pups, feeding separations as infants displayed more dis-
turbed behavior as adults.inhibits corticosterone secretion, while strok-
ing suppresses ACTH secretion. Moreover, What is known about the influence of early
postnatal stress on human development? Re-the attenuating effects of tactile stimulation
appear to be specific to maternal stimulation searchers have investigated how the mother
infant relationship affects cortisol levels by(Stanton & Levine, 1990).
Similar research with nonhuman primates exploring the relationship between attachment
security and cortisol reactivity. Nachmias,has shown that plasma cortisol increases fol-
lowing maternal separation as a function of its Gunnar, Mangelsdorf, Parritz, and Buss
(1996) reported that a secure attachment rela-duration (Levine & Wiener, 1988). In nonhu-
man primates, the presence of a familiar so- tionship buffers the cortisol responses of be-
haviorally inhibited 18-month-olds to a novelcial group can serve to reduce the endocrine
effects of maternal separation. Monkeys who situation. Only the inhibited toddlers who
were also insecurely attached to their motherswere separated from their mothers and then
isolated displayed a more profound increase exhibited significant elevations in salivary
cortisol. Gunnar, Brodersen, Nachmias, Buss,in plasma cortisol levels and a slower return
to baseline. It has been hypothesized that the and Rigatuso (1996) found that attachment se-
curity moderates the cortisol response of 15-lower stress response in the presence of a fa-
miliar social group reflects the continued month-olds to inoculation distress. Fearful
toddlers who were also insecurely attachedavailability of a stable, predictable social en-
vironment (Levine & Wiener, 1988). exhibited elevated cortisol levels. These data
suggest that, especially for temperamentallyImportantly, animal studies involving both
rodents and nonhuman primates indicate that inhibited or fearful children, sensitive, respon-
sive caretaking may be an important factor inthe effects of maternal separation can persist
into adulthood (Anisman, Zaharia, Meaney, & the modulation of the HPA axis.
One of the most profound, long-term natu-Merali, 1998; Ladd, Owens, & Nemeroff,
1996; Plotsky & Meaney, 1993). Ladd et al. ralistic studies of early deprivation has oc-
curred with Romanian orphanage children.(1996) found that adult rats who had been ma-
ternally deprived showed increased baseline These children experienced significant depri-
vation until their adoption into homes in Eu-and stress-induced plasma ACTH concentra-
G. Dawson, S. B. Ashman, and L. J. Carver702
rope, Canada, and the United States. About Lynch, & Fielding, 1993; Grunebaum,
Cohler, Kaufman, & Gallant, 1978; Hammen,6 years after adoption, Gunnar and Chisholm
(1999) examined the effects of early institu- Burge, Burney, & Adrian, 1990; Orvaschel,
WelshAllis, & Weijai, 1988; Redding, Har-tional rearing on cortisol levels and attach-
ment quality. They found that children who mon, & Morgan, 1990). By early childhood,
children of depressed mothers have a 29%had experienced 8 or more months of institu-
tional rearing had significantly higher salivary chance of developing an emotional or behav-
ioral disorder, compared to an 8% chance forcortisol compared to sex, age, and socioeco-
nomic status matched controls and compared children of medically ill parents (Hammen et
al., 1990). Later, we will review evidence thatto children who had experienced 4 or fewer
months of institutional life. Also, there was a maternal depression is associated not only
with risk for maladaptive behavior but alsosignificant positive correlation between eve-
ning cortisol levels and time in institution, with risk for alterations in brain activity.
The behavioral disturbances associatedsuggesting that the longer exposure to depri-
vation is related to greater effects on the HPA with maternal depression are evident even in
young infants. Infants of depressed mothersaxis. Moreover, securely attached institution-
alized children were more likely to show nor- tend to be withdrawn and less active and to
display lower levels of positive affect (Field,mal cortisol levels.
1986, 1992; Field, Healy, Goldstein, Perry,
Bendall, Schanberg, Zimmerman, & Kuhn,
Effects of maternal depression
1988; Field, Healy, Goldstein, & Guthertz,
1990). They also have difficulty sustainingBruer argues that examples involving such
unusual and severe deprivation as occurs in their attention and exhibit poor mastery moti-
vation (RadkeYarrow, Cummings, Kuczyn-the studies of children in orphanages cited
above do not really bear upon the concerns ski, & Chapman, 1985; ZahnWaxler, Cum-
mings, McKnew, & RadkeYarrow, 1984).that typical parents might have about the ap-
propriate kinds of emotional stimulation and Cognitive and language delays have been ob-
served by 1 year of age (RadkeYarrow et al.,responsiveness they should provide their chil-
dren. But, in fact, even less extreme variations 1985; ZahnWaxler et al., 1984).
Thus, it appears that maternal depressionin early parenting related to the parent’s own
emotional well-being appear to have signifi- may have adverse consequences on a young
infant’s early development and increase thecant long-term influence on children’s emo-
tional development, and possibly on their risk for affective or behavioral disorder in
childhood (Hammen et al., 1990). The biolog-brain development as well. Evidence for this
comes from studies of the effects of maternal ical and social mechanisms mediating these
effects are not yet understood. One proposeddepression, which is a fairly common risk fac-
tor for children, even for those children who mechanism involves the influence of the
mother’s depression on her ability to interactgrow up in otherwise advantaged environ-
ments. Children of mothers experiencing af- with her infant in a way that facilitates emo-
tional and cognitive development. Numerousfective disorders, including depression and bi-
polar disorder, during the early postnatal studies have shown that a mother experienc-
ing depression is less likely to interact in anyears are at risk for developing problems in
self-regulation, peer relationships, and sleep adaptive way with her young infant. De-
pressed mothers often find it difficult to pro-regulation, and for having behavioral prob-
lems, academic difficulties, and affective dis- vide contingent responses and optimal levels
of stimulation, and tend to show less positiveorders (Alpern & LyonsRuth, 1993; Coghill,
Caplan, Alexandra, Robson, & Kumar, 1986; and more negative affect when interacting
with their infants (Cohn, Matias, Tronick,Denham, ZahnWaxler, Cummings, & Ian-
notti, 1991; Downey & Coyne, 1990; Erick- Connell, & LyonsRuth, 1986; Cohn & Tron-
ick, 1989; Field et al., 1988, 1990; Field,son, Sroufe, & Egeland, 1985; Ghodsian, Zaj-
icek, & Wolkind, 1984; Goodman, Brogan, Sandberg, Garcia, VegaLahr, Goldstein, &
Role of experience 703
Guy, 1985). During motherinfant interac- emotion and attention regulation and that poor
regulatory skills contribute to several differenttions, there is less frequent sharing of positive
emotional states and more frequent matching types of psychopathology (Dawson, 1994).
Furthermore, there is increasing evidence thatof negative emotional states (Field et al.,
1990). parents play a central role in facilitating the
development of self-regulatory skills in youngWhen the child reaches toddlerhood, it has
been found that toddlers of depressed mothers infants and children (Cicchetti, Ganiban, &
Barnett, 1991; Malatesta & Haviland, 1982;are less likely to maintain interactions and
display less coordinated interactions. Toddlers Tronick & Gianino, 1986; Tronick, 1989). In
the case of maternal depression, it is likelyof depressed mothers have also been found to
display fewer positive affiliative behaviors to- that the inability to provide adequate positive
emotion and regulatory input affects not onlyward their mothers and higher levels of hos-
tile and aggressive behavior (Dawson, Frey, the infant’s behavioral regulation abilities but
also the brain systems that underlie these abil-Self, Panagiotides, Hessl, Yamada, & Rinaldi,
1999). Depressed mothers also are less likely ities (Dawson, 1994).
Although the studies described above haveto repair interrupted interactions (Jameson,
Gelfand, Kulcsar, & Teti, 1997). When inter- focused on the role of the depressed mother’s
behavior, other mechanisms mediating the ef-acting with their preschool-aged children, de-
pressed mothers have been found to use a less fects of maternal depression on children must
be considered. Research has shown, for exam-positive tone, display more negative affect,
express more anxiety, and provide fewer di- ple, that neonates born to depressed mothers
tend to be less active, less socially responsive,rect commands (Cox, Puckering, Pound, &
Mills, 1987; Kochanska, Kuczynski, & Ma- and fussier than those born to nondepressed
mothers (Field et al., 1985; Whiffen & Gott-guire, 1989; RadkeYarrow, Nottelmann,
Belmont, & Welsh, 1993). lib, 1989; Zuckerman, Als, Bauchner, Par-
ker, & Cabral, 1990). Prenatal exposure toTo explain the effect of maternal depres-
sion on children’s behavior, some investiga- maternal depression may be associated with a
less than optimal intrauterine environment.tors have suggested that children may be imi-
tating the mother’s depressed behavior. The contribution of genetic factors that in-
crease risk for depression is another importantOthers have hypothesized that children of de-
pressed mothers may fail to develop adequate factor, although it is unlikely that genetic fac-
tors alone can account for the high risk formeans for regulating arousal and negative af-
fect because of the mother’s difficulty in pro- emotional and behavioral disturbances found
in children of depressed mothers (Moldin,viding appropriate levels of stimulation, re-
sponsiveness, and arousal modulation. Later, Reich, & Rice, 1991; Todd, Neuman, Geller,
Fox, & Hickok, 1993).in toddlerhood, these mothers may have diffi-
culty helping the young child to develop ade- There is some evidence that the first few
years of life may represent a time of increasedquate self-regulatory strategies, leading to
maladaptive affective, attentional, social, and vulnerability for enduring effects of maternal
depression (Alpern & LyonsRuth, 1993).cognitive behavior. Early in the toddler years,
a major achievement is the ability to inhibit Wolkind, ZajicekColeman, and Ghodsian
(1980) reported that maternal depression oc-inappropriate responses and the use of self-
generated mental images to guide appropriate curring when the infants were 14 months old
was predictive of later behavioral problemsbehavior. For example, Piaget’s A not B task,
believed to be an early prefrontal task that re- during the preschool years, even when the de-
pression was absent by the time the childrenquires both inhibition of a prepotent response
and working memory to guide behavior, is were in preschool. Coghill and colleagues
(1986) found that maternal depression duringachieved some time in the 2nd year of life
(Diamond & GoldmanRakic, 1989). It has the infant’s 1st year of life was predictive of
lower cognitive ability at 4 years of age, re-been hypothesized that inhibitory skills medi-
ated by the frontal lobe play a central role in gardless of mother’s depression status when
G. Dawson, S. B. Ashman, and L. J. Carver704
the child was 4 years old. Similarly, Alpern tively structured conditions. Thus, it does not
appear that the differences in brain activityand LyonsRuth (1993) found that infants of
mothers who were depressed when their in- were simply the result of differences in the
infants’ patterns of emotional expression dur-fants were 1824 months but not depressed
when their children were 5 years were never- ing EEG recording.
Dawson and her coworkers also examinedtheless at increased risk for anxiety symptoms
at age 5 years. the relation between individual differences in
frontal brain activity and infant behavior,As stated earlier, children of depressed
mothers are not only a higher risk for cogni- which were observed in naturalistic situations
involving motherinfant play outside the psy-tive, social, and affective disturbances; they
also exhibit changes in brain activity early in chophysiology laboratory. Based on previous
theoretical and experimental work linking thelife. Dawson and colleagues have demon-
strated that 13- to 15-month-old infants of de- left frontal region with approach behaviors
and the right frontal region with withdrawalpressed mothers show reduced electrical brain
activity over the left frontal scalp region, as behaviors (Davidson, Ekman, Saron, Sen-
ulis, & Freisen, 1990; Fox, 1991), it was pre-compared to infants of nondepressed mothers
(Dawson, GroferKlinger, Panagiotides, Hill, dicted that reduced left frontal activity would
be related to lower frequencies of positive ap-& Spieker, 1992; Dawson, Frey, Panagiotides,
Osterling, & Hessl, 1997). This finding has proach behaviors in the infants. In addition,
based on a previous finding from our labora-been demonstrated in two independent sam-
ples, one involving teenaged mothers with tory that infants of depressed mothers also
show increased generalized frontal activationmultiple risk factors and another involving
middle-income, primarily married, adult during the expression of negative emotions
(Dawson, Panagiotides, GroferKlinger, &mothers who were carefully screened for a va-
riety of other risk factors that could poten- Spieker, 1997), it was predicted that increased
levels of generalized frontal activation wouldtially influence infant behavior and brain ac-
tivity (e.g., other major psychiatric disorders, be related to increased levels of intense nega-
tive affect.substance abuse, contact with Child Protective
Services, and prenatal and birth difficulties). In this study (Dawson, Frey, Self, et al.,
1999), it was found that infants of depressedIn the latter longitudinal study involving 159
mothers and their infants, Dawson and col- mothers were less affectionate and less likely
to touch their mothers during free play. Theyleagues (1997) found that infants’ atypical
frontal electroencephalogram (EEG) patterns also had more difficulty quietly occupying
themselves while their mothers filled out awere linearly related to the severity of mater-
nal depression. Interestingly, infant frontal questionnaire, and thus appeared to have more
difficulty with self-regulation. Reduced leftEEG patterns were not found to be related to
mothers’ levels of anxiety or hostility, even frontal activity was correlated with lower lev-
els of positive approach behaviors (affectionthough depressed mothers reported signifi-
cantly higher levels of these symptoms (Daw- toward mother during free play) and higher
frequencies of negative bids for attentionson et al., 1997). It was also found that the
pattern of atypical frontal electrical brain ac- (grabbing mother’s clipboard or pen while she
attempted to fill out questionnaire). In addi-tivity in infants of depressed mothers general-
ized to a range of situations in which we re- tion, increased generalized frontal brain activ-
ity was associated with higher levels of nega-corded brain activity, including a “nonsocial”
baseline condition and a standardized playful tive affect, hostility, tantrums, and aggression.
Thus, the behaviors that were found to be as-condition carried out with a familiar experi-
menter (Dawson, Frey, Panagiotides, Ya- sociated with frontal brain activity appear to
reflect the dimensions of positive approachmada, Hessl, & Osterling, 1999). Importantly,
infants of depressed and nondepressed moth- and affiliative behaviors and regulation of
negative emotions. These findings suggesters were not found to differ in terms of their
affective behavior during these brief, rela- that maternal depression is associated with al-
Role of experience 705
terations in infant brain activity and that atyp- evaluate assumptions at the intersection of
science, policy, and clinical practice. First, theical frontal brain activity is associated with
lower levels of approach behaviors and in- current state of scientific findings on the issue
must be understood. Second, reasonablecreased intensity of negative affect or diffi-
culty in regulating negative affect. hypotheses can be generated as logical exten-
sions of these scientific findings. Finally, un-Dawson (1999) also found that mothers ex-
periencing depression displayed higher levels warranted assertions need to be assessed.
Such an analysis can then lead to well-justi-of insensitive behaviors when interacting with
their infants. Insensitive behaviors broadly in- fied policy recommendations. Let us consider
such an analysis and its implications for socialcluded behaviors that reflected a difficulty in
sensitively following the cues of the infant, policy recommendations.
Regarding the current state of the science,including behaviors such as poking, tickling,
responding to infant’s bid for attention by critics agree that from the perspective of es-
tablished scientific knowledge our under-withdrawing from or rejecting solicited physi-
cal contact, and unsolicited holding. Further- standing of the neurobiology of the effects of
early experience on developmental outcome ismore, path analyses indicated that mother’s
insensitivity with her infant mediated the rela- still in its infancy (Bruer, 1999; Nelson,
1999a, 1999b; Shonkoff, in press). Neverthe-tion between maternal depression and infant
frontal EEG activity (Dawson, 1999). These less, a number of reasonable assertions and
hypotheses can be generated from what isresults provide support for the hypothesis that
the behavior of a depressed mother toward her known based on both brain and behavioral
science. First, it is clear that the prenatal andinfantin particular, the degree of maternal
insensitivitycan influence patterns of infant early postnatal years are a time during which
remarkable growth in multiple domains offrontal brain activity. Specifically, high levels
of maternal insensitivity appear to be associ- functioning (e.g., social, linguistic, cognitive,
motor) occurs in terms of both brain and be-ated with lower levels of infant left frontal
electrical brain activity. These results, taken havioral development. Second, ample evi-
dence exists indicating that these years likelytogether with previous studies on the effects
of maternal depression on infant behavior and represent a sensitive period with respect to the
effects of nutrition, exposure to toxins, andbrain activity, suggest that relatively common
variations in early parenting that are related to possibly stress. Third, this period also seems
to represent a sensitive period with respect toa parent’s emotional well-being are associated
with alterations in infant brain activity and be- the long-term beneficial effects of early inter-
vention on brain and behavioral developmenthavior. Other studies have shown that mater-
nal depression early in life is a risk factor for for some genetically based disorders, such as
PKU and autism. Fourth, evidence suggestslater psychopathology in childhood (Good-
man & Gotlib, 1999). The question of that parental mental health during the first
years of life is a significant factor with respectwhether altered brain activity early in life
constitutes a risk factor for later psychopath- to early brain activity and behavior and long-
term behavioral outcome. This paper has fo-ology is as yet unanswered and is currently
being addressed in a longitudinal study being cused on early stress and maternal depression,
but similar evidence exists with respect to theconducted by Dawson and colleagues.
influence of other forms of maladaptive par-
enting, such as maltreatment (DeBellis, Kes-
Implications for Social Policy and
havan, Clark, Casey, Giedd, Boring, Frus-
Future Research
taci, & Ryan, 1999; Pollak, Cicchetti,
Klorman, & Brumaghim, 1997).What can we say about the effects of early
experience on brain development and later Understanding the factors that determine
social and emotional outcome in humans is aoutcome and their implications for social pol-
icy? Shonkoff (in press) outlined three levels complex task that requires integrating infor-
mation about the genetic, physical, and socialof analysis that should be applied to critically
G. Dawson, S. B. Ashman, and L. J. Carver706
environment. Outcome is variable because of 1999). As Cicchetti and Cannon (1999) point
out, our hopes of finding new avenues for in-the nondeterministic, probabilistic nature of
development. As Cicchetti and Cannon (1999) tervention rest on discovery of the mecha-
nisms that constrain plasticity and change.state, “Epigenesis is viewed as probabilistic
rather than predetermined or preformational, Early development is a period that is com-
prised of many fundamental “experience ex-with the bidirectional and transactional nature
of genetic, neural, behavioral, and environ- pectant” processes. Unfortunately, there are
many conditions, such as autism, in which ge-mental influence over the life course captur-
ing the essence of probabilistic epigensis” (p. netic or acquired brain abnormalities preclude
having a normal experience of an otherwise377). Although early experiences are impor-
tant for later outcome, this does not imply that normal environment. As described by Black
et al. (1998), neuropathology can result inthe effects of any one type of early experience
are necessarily causal or permanent. Systems
theory principles such as the notion that mul-
...adevelopmental “groove” that will carry devel-
opment forward. Therapeutic manipulations may
tiple pathways can converge on a common
perturb this trajectory initially, but development
outcome (equifinality) and vice versa (multifi-
will fall back into the existing track if the canaliza-
nality) are well accepted by developmental
tion is sufficiently entrenched. However, if the per-
psychopathologists and must be incorporated
turbation is large enough, then the trajectory can
into any theory about the effects of early ex-
be shifted out of one equilibrium into another, and
perience on later outcome (Cicchetti & Ro-
from there brain development will proceed down a
gosch, 1996). In developmental psychopathol-
different pathway. As development proceeds, canal-
ogy, the term “pathway” is used to refer to
ization generally deepensdevelopmental trajec-
the cumulative influence of an individual’s
tories progressively become more difficult to redi-
specific genetic makeup and experiences that
rect by experience. This perspective supports the
together operate in a complex and probabilis-
common therapeutic strategies that early interven-
tion is better than late and that more intervention
tic fashion to influence outcome (Gottlieb,
may work better than less. (pp. 4647)
1991, 1992). An experience involving a de-
pressed mother most likely is moderated by a
host of other factors, including genetic fac- The substantial effect of early intervention
has been dramatically demonstrated in thetors, other significant relationships, the child’s
intelligence and schooling, peers, and so on. case of autism. If very intensive behavioral
intervention is commenced by 2 years of age,Each individual has a unique combination of
factors influencing outcome. Thus, in most a substantial number of children with autism
show a remarkable improvement in this con-cases it is not reasonable to consider one type
of experience as having a permanent and spe- dition (see Dawson & Osterling, 1997).
Furthermore, there are many common con-cific effect on later outcome. On the other
hand, the term “pathway” implies that, at any ditions, such as exposure to stress and mater-
nal depression, in which the variation in early,point in an individual’s development, that in-
dividual has, indeed, developed along a spe- expected environment falls outside the norm,
and these conditions do appear to have an in-cific pathway involving a complex set of risk
and protective factors, and to alter this trajec- fluence on long-term outcome. Because we
have the knowledge of many early factors thattory one must intervene through planned ther-
apeutic activities that focus on changing be- promote optimal development, it is imperative
that we translate that knowledge into socialhavioral and neural patterns of conditioning,
through insight and self-will, or through ser- policy so that society can benefit from the sci-
entific knowledge that has been gained. In theendipitous advantageous experiences (a posi-
tive role model or mentor). However it oc- case of our understanding of the importance
of early experience on brain and behavioralcurs, real energy is required; it rarely, if ever,
happens spontaneously or easily. Fortunately, development, evidence from the neurosci-
ences and the behavioral sciences offers ainherent plasticity appears to be a characteris-
tic of at least some brain structures (Johnson, firm base for identifying optimal conditions
Role of experience 707
for children’s development. Public under- tervention programs for pregnant women
suffering from alcohol or drug addictionstanding of the importance of such conditions
is a critical first step that must be followed by are needed.
the design and implementation of policy and
3. Similarly, a brief assessment of mother’s
intervention efforts. There is much more we
mental health should be included as part of
do as a society to provide an optimal environ-
the regular well-baby checkups, along with
ment in the first years of life and beyond. Pol-
educational materials related to infant nutri-
icy should focus on primary prevention of ad-
tion and behavioral development. Contin-
verse outcomes by reducing known risk
ued efforts to improve identification of psy-
factors related to early environment and expe-
chopathology in infants during well-baby
rience so that such factors can be thwarted be-
checkups should also be supported.
fore they have any influence on outcome, as
well as on secondary prevention by identify-
4. Increased efforts to train health care work-
ing environmental factors that are modifiable
ers in how to detect and respond when par-
moderators or mediators of outcome so that
ents are experiencing mental health prob-
we can mitigate the negative influence of such
lems are needed.
risk factors on children’s development and
5. Communities struggling with poverty and
outcome. Specifically, we believe that the fol-
the host of associated problems that are as-
lowing policy recommendations are well jus-
sociated with poverty (stress, violence,
tified based on the current state of knowledge
poor nutrition, parental psychopathology,
regarding the effects of early experience on
impoverished educational opportunities)
brain and behavioral development.
should be a direct and substantial focus of
programs related to optimal prenatal and
1. In general, although prevention and early
early postnatal environments because chil-
intervention efforts should not exclusively
dren growing up in such communities are
focus on the earliest years of development,
most likely to be exposed to multiple risk
it is clear from the research discussed
factors that are associated with poor long-
above that such efforts should begin as
term outcome.
early as possible. By directing such efforts
6. Because the prenatal and early postnatal
toward promoting optimal prenatal and in-
years represent a sensitive period with re-
fanttoddler development, the long-term
spect to the long-term beneficial effects of
negative consequences of factors that have
early intervention on brain and behavioral
their greatest influences during early devel-
development for some genetically based
opment and which set the stage for future
disorders, such as autism, increased efforts
development can be minimized or avoided
at early identification of such disorders is
needed. Greater public awareness and edu-
2. Prevention efforts that promote healthy pre-
cation of health care providers with respect
natal development should focus on increas-
how to detect developmental disorders dur-
ing public awareness, outreach efforts, and
ing infancy and toddlerhood and how to fa-
intervention programs related to improving
cilitate access to appropriate interventions
prenatal nutrition, reducing fetal exposure
are needed.
to toxins (alcohol, drugs), and minimizing
maternal stress and psychopathology dur- 7. Efforts aimed at early identification, pre-
vention, and remediation of developmentaling pregnancy. In light of findings that pre-
natal depression and stress can influence disorders should be enhanced. To provide
one example, autism has become recog-fetal and neonatal behavior, prenatal
screening should include a brief assessment nized as a relatively prevalent (1 in 500
1000 persons) developmental disorder thatof maternal mental health so that appro-
priate medical or psychological interven- can and should be detected during infancy
in most cases (Osterling & Dawson, 1994,tions can begin at this time. Moreover, in-
G. Dawson, S. B. Ashman, and L. J. Carver708
1999). Unfortunately, autism is not typi- tribution of parenting factors to the devel-
opment of self-regulatory brain mecha-cally diagnosed in children until around the
age of 34 years (Siegel, Pliner, Eschler, & nisms that have been hypothesized to relate
to affective and attentional disorders is stillElliot, 1988). Pediatricians and other health
care professionals need to be aware of how poorly understood.
to assess early symptoms of autism in in-
3. It needs to be determined whether psycho-
fants and toddlers so that appropriate
biological measures such as neuropsycho-
screening and referral can occur. Moreover,
logical performance, cortisol levels, auto-
given the dramatic impact of early interven-
nomic responses, and brain electrical
tion in autism, funding for early behavioral
activity will be useful in identifying chil-
intervention programs for infants and tod-
dren at risk for psychopathology.
dlers at risk for autism is clearly justified
and cost effective.
4. Continued research on the neurobiological
bases of different types of child psycho-
8. In general, financial, emotional, and practi-
pathology will be important for understand-
cal support needs to be provided to families
ing the etiology, nature, and treatment of
who are struggling to access appropriate in-
such disorders. Such research will lay the
tervention for their children who have been
foundation for identifying phenotypic
identified as having a developmental disor-
markers for childhood disorders, which will
der, chronic illness, or mental health prob-
be essential for early identification, design-
lem. Denial of such support to families by
ing interventions, and discovering genetic
insurance companies and government agen-
cies is shortsighted on the part of these
health care systems in light of what is
5. There is also a need to develop neurobio-
known about the critical impact of early in-
logical frameworks for interventions for
tervention on long-term outcome.
children at risk for psychopathology be-
cause of genetic or environmental factors.
Future research should focus on increasing
For example, the use of neurocognitive and
our understanding of the multiple influences
psychophysiological assessments that target
on children’s development and outcome, and
specific brain regions, such as prefrontal
thus will depend upon multidisciplinary, lon-
functioning, may allow us to design indi-
gitudinal approaches that integrate biological
vidualized treatment approaches based on
and environmental factors. Among the impor-
neurobiological frameworks.
tant issues that need to be addressed in future
research are the following:
6. Similarly, measures of response to inter-
ventions should include neuropsychological
1. Given that different biological systems de-
and psychophysiological indices of brain
velop on different timetables, it needs to be
function to determine whether and how
determined whether and how specific envi-
specific brain systems may be influenced
ronmental events, such as exposure to
by interventions.
stress and maternal depression, selectively
affect the development of specific neurobi-
7. The degree of plasticity in neural systems
ological systems depending on the timing
as it relates to risk for child psychopathol-
and duration of the exposure to such events
ogy needs to be understood. For example,
and whether and how timing influences risk
issues related to timing, duration, and type
for psychopathology. In particular, studies
of early interventions that may influence
that address these issues in humans are
outcome in children at risk for psychopath-
ology need to be explored.
2. The role of the environment in promoting
optimal brain function in children needs to In conclusion, technological advances in
brain research continue to make this an excit-be better understood. For example, the con-
Role of experience 709
ing time with respect to our ability to under- ing of brain and behavioral development but
rather the translation of that knowledge intostand the neural bases of normal and abnor-
mal development. As science continues to meaningful policy and action. This responsi-
bility, shared by the general public, scientists,move this effort forward at a remarkably fast
pace, it has become apparent that our most practitioners, and policymakers, should be a
central focus of our efforts.difficult challenge will not be the understand-
Alpern, L., & LyonsRuth, K. (1993). Preschool children mammalian brain. Annual Review of Neuroscience,
1997, 157184.
at social risk: Chronicity and timing of maternal de-
Cicchetti, D., & Cannon, T. D. (1999). Neurodevelop-
pressive symptoms and child behavior at school and
mental processes in the ontogenesis and epigenesis of
at home. Development and Psychopathology, 5, 371
psychopathology. Development and Psychopathology,
11, 375393.
Anisman, H., Zaharia, M. D., Meaney, M. J., & Merali,
Cicchetti, D., Ganiban, J., & Barnett, D. (1991). Contri-
Z. (1998). Do early-life events permanently alter be-
butions from the study of high risk populations to un-
havioral and hormonal responses to stressors? Inter-
derstanding the development of emotion regulation.
national Journal of Developmental Neuroscience, 16,
In K. Dodge & J. Garber (Eds.), The development of
emotion regulation (pp. 1548). New York: Cam-
Barad, M., Bourtchouladze, R., Winder, D. G., Golan,
bridge University Press.
H., & Kandel, E. R. (1998). Rolipram, a type IV-spe-
Cicchetti, D., & Rogosch, F. A. (1996). Equifinality and
cific phosphodiesterase inhibitor, facilitates the estab-
multifinality in developmental psychopathology. De-
lishment of long-lasting long-term potentiation and
velopmental Psychopathology, 8, 597600.
improves memory. Proceedings of the National Acad-
Clarke, A. S., Wittwer, D. J., Abbott, D. H., & Schneider,
emy of Sciences, USA, 95, 1502015025.
M. L. (1994). Long-term effects of prenatal stress on
Bell, M. A., & Fox, N. A. (1994). Brain development
HPA axis activity in juvenile rhesus monkeys. Devel-
over the first year of life: Relations between EEG fre-
opmental Psychobiology, 27, 257269.
quency and coherence and cognitive and affective be-
Coghill, S. R., Caplan, H. L., Alexandra, H., Robson,
haviors. In G. Dawson & K. Fischer (Eds.), Human
K., & Kumar, R. (1986). Impact of maternal postnatal
behavior and the developing brain (pp. 314345).
depression on cognitive development of young chil-
New York: Guilford Press.
dren. British Medical Journal, 292, 11651167.
Black, J. E., Jones, T. A., Nelson, C. A., & Greenough,
Cohn, J. F., Matias, R., Tronick, E. Z., Connell, D., &
W. T. (1998). Neuronal plasticity and the developing
LyonsRuth, D. (1986). Face-to-face interactions of
brain. In N. E. Alessi, J. T. Coyle, S. I. Harrison, &
depressed mothers and their infants. In E. Z. Tron-
S. Eith (Eds.), Handbook of child and adolescent psy-
ick & T. Field (Eds.), Maternal depression and infant
chiatry: Vol 6. Basic psychiatric science and treat-
disturbance (pp. 3145). San Francisco: JosseyBass.
ment (pp. 3153). New York: Wiley.
Cohn, J. F., & Tronick, E. Z. (1989). Specificity of in-
Bourgeois, J. P., Jastreboff, P., & Rakic, P. (1989). Syn-
fants’ response to mothers’ affective behavior. Jour-
aptogenesis in the visual cortex of normal and pre-
nal of the American Academy of Child and Adolescent
term monkeys: Evidence of the intrinsic regulation of
Psychiatry, 28, 242248.
synaptic overproduction. Proceedings of the National
Comery, T. A., Harris, J. B., Willems, P. J., Oostra,
Academy of Sciences, 86, 42974301.
B. A., Irwin, S. A., Weiler, I. J., & Greenough, W. T.
Bourtchouladze, R., Frenguelli, B., Blendy, J., Cioffi, D.,
(1997). Abnormal dendritic spines in Fragile X
Schutz, G., & Silva, A. J. (1994). Deficient long-term
knockout mice: Maturation and pruning deficits. Pro-
memory in mice with a targeted mutation of the
ceedings of the National Academy of Sciences, 94,
CAMP-responsive element-binding protein. Cell, 79,
Coplan, J. D., Andrews, M. W., Rosenblum, L. A., Ow-
Bruer, J. T. (1999). The myth of the first three years: A
ens, M. J., Friedman, S., Gorman, J. M., & Nemeroff,
new understanding of early brain development and
C. B. (1996). Persistent elevations of cerebrospinal
lifelong learning. New York: Free Press.
fluid concentrations of corticotropin-releasing factor
Campbell, F. A., & Ramey, C. T. (1994). Effects of early
in adult nonhuman primates exposed to early-life
intervention on intellectual and academic achieve-
stressors: Implications for the pathophysiology of
ment: A follow-up study of children from low-income
mood and anxiety disorders. Proceedings of the Na-
families. Child Development, 65, 684698.
tional Academy of Sciences, 93, 16191623.
Capitanio, J. P., Rasmussen, K. L. R., Snyder, D. S.,
Cox, A. D., Puckering, C., Pound, A., & Mills, M.
Laudenslager, M., & Reite, M. (1986). Long-term fol-
(1987). The impact of maternal depression in young
low-up of previously separated pigtail macaques:
children. Journal of Child Psychology and Psychia-
Group and individual differences in response to novel
try, 28, 917928.
situations. Journal of Child Psychology and Psychia-
Davidson, R. J., Ekman, P., Saron, C., Senulis, R., &
try, 27, 531538.
Friesen, W. V. (1990). Approachwithdrawal and ce-
Chen, C., & Tonegawa, S. (1997). Molecular genetic
rebral asymmetry: Emotional expression and brain
analysis of synaptic plasticity, activity-dependent
physiology I. Journal of Personality and Social Psy-
chology, 58, 330341.neural development, learning, and memory in the
G. Dawson, S. B. Ashman, and L. J. Carver710
Dawson, G. (1994). Frontal electroencephalographic cor- logical theory of consciousness. New York: Basic
Books.relates of individual differences in emotional expres-
sion in infants: A brain systems perspective on emo- Erickson, M., Sroufe, L. A., & Egeland, B. (1985). The
relationship between quality of attachment and behav-tion. Monographs of the Society for Research In Child
Development, 59(2/3), 135151. ior problems in preschool in a high-risk sample.
Monographs of the Society for Research in Child De-Dawson, G. (1999). The effects of maternal depression
on children’s emotional and psychobiological devel- velopment, 50(1/2), 147166.
Fameli, M., Kitraki, E., & Stylianopoulou, F. (1994). Ef-opment. Paper presented at a 1999 National Institutes
of Health Conference on Parenting, Bethesda, MD. fects of hyperactivity of the maternal hypothalamic
pituitaryadrenal (HPA) axis during pregnancy on theDawson, G., & Fischer, K. W. (Eds.). (1994). Human be-
havior and the developing brain. New York: Guilford development of the HPA axis and brain monoamines
of the offspring. International Journal of Develop-Press.
Dawson, G., Frey, K., Panagiotides, H., Osterling, J., & mental Neuroscience, 12, 651659.
Field, T. (1986). Models for reactive and chronic depres-Hessl, D. (1997). Infants of depressed mothers exhibit
atypical frontal brain activity: A replication and ex- sion in infancy. In E. Z. Tronick & T. Field (Eds.),
Maternal depression and infant disturbance (pp. 47tension of previous findings. Journal of Child Psy-
chology and Psychiatry, 38, 179186. 60). San Francisco: JosseyBass.
Field, T. (1992). Infants of depressed mothers. Develop-Dawson, G., Frey, K., Panagiotides, H., Yamada, E.,
Hessl, D., & Osterling, J. (1999). Infants of depressed ment and Psychopathology, 4, 4966.
Field, T., Healy, B., Goldstein, S., & Guthertz, M. (1990).mothers exhibit atypical frontal electrical brain activ-
ity during interactions with mother and with a famil- Behaviorstate matching and synchrony in mother
infant interactions of non-depressed versus depressediar, nondepressed adult. Child Development, 70,
10581066. dyads. Developmental Psychology, 26, 714.
Field, T., Healy, B., Goldstein, S., Perry, S., Bendall, D.,Dawson, G., Frey, K., Self, J., Panagiotides, H., Hessl,
D., Yamada, E., & Rinaldi, J. (1999). Frontal electri- Schanberg, S., Zimmerman, E., & Kuhn, C. (1988).
Infants of depressed mothers show “depressed” be-cal brain activity in infants of depressed mothers: Re-
lation to variations in infant behavior. Development havior even with non-depressed adults. Child Devel-
opment, 59, 15691579.and Psychopathology, 11, 589605.
Dawson, G., GroferKlinger, L., Panagiotides, H., Hill, Field, T., Sandberg, D., Garcia, R., VegaLahr, N., Gold-
stein, S., & Guy, L. (1985). Prenatal problems, post-D., & Spieker, S. (1992). Frontal lobe activity and
affective behavior of infants of mothers with depres- partum depression, and early motherinfant interac-
tions, Developmental Psychology, 12, 11521156.sive symptoms. Child Development, 63, 725737.
Dawson, G., & Osterling, J. (1997). Early intervention Fox, N. A. (1991). If it’s not left, it’s right: Electroen-
cephalograph asymmetry and the development ofin autism: Effectiveness and common elements of
current approaches. In Guralnick, M. J. (Ed.), The ef- emotion. American Psychologist, 46, 863872.
Fride, E., & Weinstock, M. (1989). Alterations in behav-fectiveness of early intervention: Second generation
research (pp. 307326). Baltimore, MD: Brookes. ioral and striatal dopamine asymmetries induced by
prenatal stress. Pharmacological Biochemical Behav-Dawson, G., Panagiotides, H., GroferKlinger, L., &
Spieker, S. (1997). Infants of depressed and nonde- ior, 32, 425430.
Ghodsian, M., Zajicek, E., & Wolkind, S. (1984). A lon-pressed mothers exhibit differences in frontal brain
electrical activity during the expression of negative gitudinal study of maternal depression and child be-
havior problems. Journal of Child Psychology andemotions. Developmental Psychology, 33, 650656.
Day, J. C., Koehl, M., Deroche, V., Le Moal, M., & Mac- Psychiatry, 25, 91109.
Glover, V. (1997). Maternal stress or anxiety in preg-cari, S. (1998). Prenatal stress enhances stress- and
corticotropin-releasing factor-induced stimulation of nancy and emotional development of the child [Edito-
rial]. The British Journal of Psychiatry, 171, 105hippocampal acetylcholine release in adult rats. Jour-
nal of Neuroscience, 18, 18861892. 106.
Goodman, S. H., Brogan, D., Lynch, M. E., & Fielding,DeBellis, M. D., Keshavan, M. S., Clark, D. B., Casey,
B. J., Giedd, J. N., Boring, A. M., Frustaci, K., & B. (1993). Social and emotional competence in chil-
dren of depressed mothers. Child Development, 64,Ryan, N. D. (1999). A. E. Bennett Research Award.
Developmental traumatology. Part II: Brain develop- 516531.
Goodman, S. H., & Gotlib, I. H. (1999). Risk for psycho-ment. Biological Psychiatry, 45, 12711284.
Denham, S. A., ZahnWaxler, C., Cummings, E. M., & pathology in the children of depressed mothers: A de-
velopmental model for understanding mechanisms ofIannotti, R. J. (1991). Social competence in young
children’s peer relations: Patterns of development and transmission. Psychological Review, 106, 458490.
Gottlieb, G. (1991). Experiential canalization of behaviorchange. Child Psychiatry and Human Development,
22, 2944. development: Theory. Developmental Psychology, 27,
413.Diamond, A., & GoldmanRakic, P. (1989). Comparison
of human infants and rhesus monkeys on Piaget’s A- Gottlieb, G. (1992). Individual development and evolu-
tion: The genesis of novel behavior. New York: Ox-not-B task: Evidence for dependence on dorsolateral
prefrontal cortex. Experimental Brain Research, 74, ford University Press.
Greenough, W. T. (1997). We can’t just focus on ages2440.
Downey, G., & Coyne, J. (1990). Children of depressed zero to three. APA Monitor, 28, 19.
Greenough, W. T., Black, J. E., & Wallace, C. S. (1987).parents: An integrative review. Psychological Bulle-
tin, 108, 5076. Experience and brain development. Child Develop-
ment, 58, 539559.Edelman, G. M. (1987). Neural Darwinism: The theory
of neuronal group selection. New York: Basic Books. Groginsky, S., Christian, S., & McConnell, L. (1998).
Early childhood initiatives in the states: TranslatingEdelman, G. M. (1989). The remembered present: A bio-
Role of experience 711
research into policy. In State Legislative Report (Vol. maternal separation: Mechanisms and mediators. In-
23). Denver, CO: National Conference of State Legis-
ternational Journal of Developmental Neuroscience,
16, 261270.
Grunebaum, H. U., Cohler, B. J., Kaufman, C., & Gal-
Ladd, C. O., Owens, M. J., & Nemeroff, C. B. (1996).
lant, D. H. (1978). Children of depressed and schizo-
Persistent changes in corticotropin-releasing factor
phrenic mothers. Child Psychiatry and Human Devel-
neuronal systems induced by maternal deprivation.
opment, 8, 219228.
Endocrinology, 137, 12121218.
Gunnar, M. R., & Chisholm, K. C. (1999, April). Effects
Levay, S., Wiesal, T. N., & Hubel, D. H. (1980). The
of early institutional rearing and attachment quality
development of ocular dominancy columns in normal
on salivary cortisol levels in adopted Romanian chil-
and visually deprived monkeys. Journal of Compara-
dren. Poster session presented at the biennial meeting
tive Neurology, 19, 1151.
of the Society for Research in Child Development,
Levine, S., & Wiener, S. G. (1988). Psychoendocrine as-
Albuquerque, NM.
pects of motherinfant relationships in nonhuman pri-
Gunnar, M. R., Broderson, L., Nachmias, M., Buss, K., &
mates. Psychoneuroendocrinology, 13, 143154.
Rigatuso, J. (1996). Stress reactivity and attachment
Lobel, M. (1994). Conceptualizations, measurement, and
security. Developmental Psychobiology, 29, 191204.
effects of prenatal maternal stress on birth outcomes.
Hammen, C., Burge, D., Burney, E., & Adrian, C. (1990).
Journal of Behavioral Medicine, 17, 225272.
Longitudinal study of diagnoses in children of women
Lordi, B., Protais, P., Mellier, D., & Caston, J. (1997).
with unipolar and bipolar affective disorder. Archives
Acute stress in pregnant rats: Effects on growth rate,
of General Psychiatry, 47, 11121117.
learning, and memory capabilities of the offspring.
Hebb, D. O. (1949). The organization of behavior: A neu-
Physiology & Behavior, 62, 10871092.
ropsychological theory. New York: Wiley.
Lu, Y., Jia, Z., Janus, C., Henderson, J., Gerlai, R., Woj-
Huttenlocher, P. R. (1994). Synaptogenesis in human ce-
towicz, J. M., & Roder, J. C. (1997). Mice lacking
rebral cortex. In G. Dawson & K. Fischer (Eds.), Hu-
metabotropic glutamate receptor 5 show impaired
man behavior and the developing brain (pp. 137
learning and reduced CA2 long-term potentiation
152). New York: Guilford.
(LTP) but normal CA 3LTP. The Journal of Neuro-
Huttenlocher, P. R., & Dabholkar, A. S. (1997). Regional
science, 17, 51965205.
differences in synaptogenesis in human cerebral cor-
Malatesta, C. Z., & Haviland, J. M. (1982). Learning dis-
tex. Journal of Comparative Neurology, 387, 167–
play rules: The socialization of emotion expression in
infancy. Child Development, 53, 9911003.
Jacobs, B., Schall, M., & Scheibel, A. B. (1993). A quan-
Malenka, R. C., & Nicoll, R.A. (1999). Long-term poten-
titative dendritic analysis of Wernicke’s area: Gender,
tiationA decade of progress? Science, 285, 1870
hemispheric, and environmental factors. Journal of
Comparative Neurology, 237, 97111.
Mayford, M., Bach, M. E., Huang, Y., Wang, L., Haw-
Jacobs, B., & Scheibel, A. B. (1993). A quantitative den-
kins, R. D., & Kandel, E. R. (1996). Control of mem-
dritic analysis of Wernicke’s area: Lifespan changes.
ory formation through regulated expression of a
Journal of Comparative Neurology, 237, 8396.
CaMK11 Transgene. Science, 274, 16781683.
Jameson, P. B., Gelfand, D. M., Kulcsar, E., & Teti,
Meier, A. (1985). Child psychiatric sequelae of maternal
D. M. (1997). Mothertoddler interaction patterns as-
war stress. Acta Psychiatrica Scandinavica, 72, 505
sociated with maternal depression. Development and
Psychopathology, 9, 537550.
Meiri, N., Sun, M., Segal, Z., & Alkon, D. L. (1998).
Johnson, M. H. (1999). Cortical plasticity in normal and
Memory and long-term potentiation (LTP) dissoci-
abnormal development: Evidence and working
ated: Normal spatial memory despite CA1 LTP elimi-
hypotheses. Development and Psychopathology, 11,
nation with Kv1.4 antisense. Proceedings of the Na-
tional Academy of Science, USA, 95, 1503715042.
Katz, L. D., & Shatz, C. J. (1996). Synaptic activity and
Moldin, S. O., Reich, T., & Rice, J. P. (1991). Current
the construction of cortical circuits. Science, 274,
perspectives on the genetics of unipolar depression.
Behavior Genetics, 21, 211242.
Kinsley, C. H., Mann, P. E., & Bridges, R. S. (1989).
Morgan, G., & Gibson, K. R. (1991). Nutritional and en-
Alterations in stress-induced prolactin release in adult
vironmental interactions in brain development. In
female and male rats exposed to stress, in utero. Phys-
K. R. Gibson & A. C. Petersen (Eds.), Brain matura-
iological Behavior, 45, 10731076.
tion and cognitive development (pp. 91–106). New
Knudsen, E. I. (1999). Early experience and critical peri-
York: Aldine de Bruyter.
ods. Developmental Psychology, 26, 398408.
Nachmias, M., Gunnar, M., Mangelsdorf, S., Parritz,
Kochanska, G., Kuczynski, L., & Maguire, M. (1989).
R. H., & Buss, K. (1996). Behavioral inhibition and
Impact of diagnosed depression and self-reported
stress reactivity: The moderating role of attachment
mood on mothers’ control strategies: A longitudinal
security. Child Development, 67, 508522.
study. Journal of Abnormal Child Psychology, 17,
Nelson, C. A. (1999a). Neural plasticity and human de-
velopment. Current Directions in Psychological Sci-
Kolb, B., Forgie, M., Gibb, R., Gorney, G., & Rowntree,
ence, 8, 4245.
S. (1998). Age, experience and the changing brain.
Nelson, C. A. (1999b). How important are the first 3
Neuroscience & Biobehavioral Reviews, 22, 123
years of life? Applied Developmental Science, 3,
Kuhn, C. M., Pauk, J., & Schanberg, S. M. (1990). Endo-
Nelson, C. A. (Ed.). (in press). Minnesota Symposia on
crine responses to mother infant separation in devel-
Child Psychology: Vol. 31. The effects of adversity on
oping rats. Developmental Psychobiology, 23, 395
neurobehavioral development. Hillsdale, NJ: Erl-
Kuhn, C. M., & Schanberg, S. M. (1998). Responses to baum.
G. Dawson, S. B. Ashman, and L. J. Carver712
Newport, E. L. (1990). Maturational constraints on lan- Sonderegger, T. B. (Ed.). (1992). Perinatal substance
abuse. Baltimore, MD: Johns Hopkins Universityguage learning. Cognitive Science, 14, 1128.
Orvaschel, H., WelshAllis, G., & Weijai, Y. (1988). Press.
Spohr, H. L., Williams, J., & Steinhausen, H. C. (1993).Psychopathology in children of parents with recurrent
depression. Journal of Abnormal Child Psychology, Prenatal alcohol exposure and long-term develop-
mental consequences. Lancet, 341, 907910.16, 1728.
Osterling, J., & Dawson, G. (1994). Early recognition of Stanton, M. E., & Levine, S. (1990). Inhibition of infant
glucocorticoid stress response: Specific role of mater-children with autism: A study of first birthday home
video tapes. Journal of Autism and Developmental nal cues. Developmental Psychobiology, 23, 411
426.Disorders, 24, 247257.
Osterling, J., & Dawson, G. (1999). Early identification Stott, D. H. (1973). Follow-up study from birth of the
effects of prenatal stresses Developmental Medicineof one-year-old with autism versus mental retarda-
tion. Poster presented at the 1999 meeting of the Soci- and Child Neurology, 15, 770787.
Suchecki, D., Rosenfeld, P., & Levine, S. (1993). Mater-ety of Research in Child Development, Albuquerque,
NM. nal regulation of the hypothalamicpituitaryadrenal
axis in the infant rat: The role of feeding and stroking.Pihoker, C., Owens, M. J., Kuhn, C. M., Schanberg,
S. M., & Nemeroff, C. B. (1993). Maternal separation Journal of Brain Research, 75, 185192.
Thompson, R. A., & Nelson, C. A. (in press). Develop-in neonatal rats elicits activation of the hypothala-
micpituitaryadrenocortical axis: A putative role for mental science and the media: Early brain develop-
ment. American Psychologist.corticotropin-releasing factor. Psychoneuroendocrin-
ology, 18, 485493. Todd, R. D., Neuman, R., Geller, B., Fox L. W., &
Hickok, J. (1993). Genetic studies of affective disor-Plotsky, P. M., & Meaney, M. J. (1993). Early, postnatal
experience alters hypothalamic corticotropin-releas- ders: Should we be starting with childhood onset pro-
bands? Journal of the American Academy of Child &ing factor (CRF) mRNA, median eminence CRF con-
tent and stress-induced release in adult rats. Molecu- Adolescent Psychiatry, 32, 11641171.
Toni, N., Buchs, P. A., Nikonenko, I., Bron, C. R., &lar Brain Research, 18, 195200.
Pollak, S. D., Cicchetti, D., Klorman, R., & Brumaghim, Muller, D. (1999). LTP promotes formation of multi-
ple spine synapses between a single axon terminalJ. T. (1997). Cognitive brain event-related potentials
and emotion processing in maltreated children. Child and a dendrite. Nature, 402, 421425.
Tronick, E. Z. (1989). Emotions and emotional communi-Development, 68, 773787.
RadkeYarrow, M., Cummings, E. M., Kuczynski, L., & cation in infants. American Psychologist, 44, 112119.
Tronick, E. Z., & Gianino, A. F. (1986). The transmissionChapman, J. (1985). Patterns of attachment in two-
and three-year-olds in normal families and families of maternal disturbances to the infant. In E. Z. Tron-
ick & T. Field (Eds.), Maternal depression and infantwith parental depression. Child Development, 56,
884893. disturbance (pp. 511). San Francisco: JosseyBass.
Wappner, R., Cho, S., Kronmal, R. A., Schuett, V., &RadkeYarrow, M., Nottelmann, E., Belmont, B., &
Welsh, J. D. (1993). Affective interactions of de- Seashore, J. R. (1999). Management of phenylketonu-
ria for optimal outcome: A review of guidelines forpressed and nondepressed mothers and their children.
Journal of Abnormal Child Psychology, 21, 683695. phenylketonuria management and a report of surveys
of parents, patients, and clinic directors. Pediatrics,Rakic, P., Bourgeois, J. P., & GoldmanRakic, P. S.
(1994). Synaptic development of the cerebral cortex: 104, 4–9.
Weinstock, M. (1997). Does prenatal stress impair copingImplications for learning, memory, and mental illness.
Progress in brain research, 102, 227243. and regulation of hypothalamicpituitaryadrenal
axis? Neuroscience and Biobehavioral Reviews, 21,Ramsay, D. S., & Lewis, M. (1995). The effects of birth
condition on infants’ cortisol response to stress. Pedi- 110.
Weinstock, M., Fride, E., & Hertzberg, R. (1988). Prena-atrics, 95, 546549.
Redding, R. E., Harmon, R. J., & Morgan, G. A. (1990). tal stress effects on functional development of the off-
spring. In G. J. Boer, M. G. P. Feenstra, M. Mirmiran,Relationships between maternal depression and in-
fants’ mastery behaviors. Infant Behavior and Devel- D. F. Swaab, & F. Van Haaren (Eds.), Progress in
brain research (pp. 319331). Amsterdam: Elsevier.opment, 13, 391395.
Schneider, M. L. (1992a). Prenatal stress exposure alters Whiffen, V. E., & Gottlib, I. M. (1989). Infant of postpar-
tum depressed mothers: Temperament and cognitivepostnatal behavioral expression under conditions of
novelty challenge in rhesus monkey infants. Develop- status. Journal of Abnormal Psychology, 98, 274
279.mental Psychobiology, 25, 529540.
Schneider, M. L. (1992b). Delayed object permanence Wolkind, S. N., ZajicekColeman, E., & Ghodsian, M.
(1980). Continuities in maternal depression. Interna-development in prenatally stressed rhesus monkey in-
fants (Macaca mulatta). Occupational Therapy Jour- tional Journal of Family Psychiatry, 1, 167182.
ZahnWaxler, C., Cummings, E. M., McKnew, D. H., &nal of Research, 12, 96110.
Shonkoff, J. P. (in press). Science, policy, and practice: RadkeYarrow, J. (1984). Problem behaviors and
peer interactions of young children with a manicde-Three cultures in search of a shared mission. Child
Development. pressive parent. American Journal of Psychiatry, 141,
236240.Siegel, B., Pliner, C., Eschler, J., & Elliot, G. R. (1988).
How children with autism are diagnosed: Difficulties Zuckerman, B., Als, H., Bauchner, H., Parker, S., & Ca-
bral, H. (1990). Maternal depressive symptoms duringin identification of children with multiple develop-
mental delays. Developmental and Behavioral Pediat- pregnancy and newborn irritability. Developmental
and Behavioral Pediatrics, 11, 190194.rics, 9, 199204.
... Considering the possible correlation between perinatal exposure of children to maternal PMDs through cortisol levels and child behavioral disorders, it was found that PMD mothers evaluated attention deficit/hyperactivity problems with higher scores in the CBCL scale. Previous studies have shown that maternal emotional disorders, especially during the postpartum period, have negative effects on children, such as attention problems [27]. Van Batenburg-Eddes et al. [28] reported a strong association between antenatal anxiety disorders and childhood disorders. ...
Full-text available
Maternal perinatal mental disorders (PMD) are associated with developmental and behavioral problems in children, probably mediated by the programming of the hypothalamic–pituitary–adrenal (HPA) axis. Increased cortisol concentrations during the antenatal and perinatal periods have been related to long-term effects on children’s behavior and stress response. We aimed to investigate the association of hair cortisol concentrations (HCC) between mothers, with (n = 16) and without PMD (n = 30), and their children, aged between 18 and 48 months. Participants were evaluated with a clinical interview and questionnaires for the Depression Anxiety Stress Scale and the Child Behavior Checklist for ages 1½–5. Maternal and child HCCs were compared between the two groups. Children of the PMD group had increased symptoms of attention deficit hyperactivity disorder. A positive linear association between maternal and child HCC was observed only in the total sample of mother–child dyads and the control group. In the PMD group, children’s HCCs were significantly associated with child anxiety/depression symptoms. Aggressive behavior and oppositional/defiant problems correlated significantly with children’s own HCCs, and their mother’s too. These findings suggest that a chronic dysregulation of maternal and child HPA axis and their associations in the PMD dyads may underlie the linkage among prolonged maternal stress, child behavioral/emotional problems and stress responses.
... The DOHaD paradigm [27] states that prenatal maternal stress can negatively affect pregnancy outcomes and fetal developmental processes, including neurogenesis, neural migration, and myelination [86]. Adverse outcome of these fetal neurodevelopmental processes are associated with an increased risk of developing mental and physiological disorders later in life, such as autism spectrum disorder and attention-deficit/hyperactivity disorder [26,87]. For example, maternal prenatal stress associated with the potential prospect of deportation in pregnant Latina women during the 2016 USA presidential election appeared to be associated with an increase in the incidence of preterm birth among these women [88], and the offspring of pregnant women who developed posttraumatic stress disorder (PTSD) due to the terrorist attacks on the World Trade Center showed lower levels of cortisol when compared to the offspring of mothers who did not. ...
Full-text available
The COVID-19 pandemic has a major impact on society, particularly affecting its vulnerable members, including pregnant women and their unborn children. Pregnant mothers reported fear of infection, fear of vertical transmission, fear of poor birth and child outcomes, social isolation, uncertainty about their partner’s presence during medical appointments and delivery, increased domestic abuse, and other collateral damage, including vaccine hesitancy. Accordingly, pregnant women’s known vulnerability for mental health problems has become a concern during the COVID-19 pandemic, also because of the known effects of prenatal stress for the unborn child. The current narrative review provides a historical overview of transgenerational effects of exposure to disasters during pregnancy, and the role of maternal prenatal stress. We place these effects into the perspective of the COVID-19 pandemic. Hereby, we aim to draw attention to the psychological impact of the COVID-19 pandemic on women of reproductive age (15–49 year) and its potential associated short-term and long-term consequences for the health of children who are conceived, carried, and born during this pandemic. Timely detection and intervention during the first 1000 days is essential to reduce the burden of transgenerational effects of the COVID-19 pandemic.
... There is a broad consensus among researchers that different types of early experience can have both positive and negative effects on later behavior in a wide variety of species, including rodents (Pryce and Feldon, 2003;Baldini et al., 2013), cats (Casey and Bradshaw, 2008), horses (Lansade et al., 2005), foxes (Pedersen and Jeppesen, 1990), pigs (Weaver et al., 2000;Day et al., 2002;Zupan et al., 2016), primates (Suomi, 1997), dogs (Gazzano et al., 2008;Tiira and Lohi, 2015;Harvey et al., 2016;Vaterlaws-Whiteside and Hartmann, 2017;Dietz et al., 2018;Hunt and Vaterlaws-Whiteside, 2020), and humans (Dawson et al., 2000;Gunnar and Reid, 2019). The effects of the early experience can be positive or negative depending on the type and intensity of the early experience and on the tests used to measure these effects (Fox and Stelzner, 1966;Pryce and Feldon, 2003;Raineki et al., 2014). ...
Early Neurological Stimulation (ENS) has been defined as the application of five specific brief daily manipulations to pups from birth until 2 to 3 weeks of age (Battaglia, 2009). This approach has been adopted by many kennels and promoted as a means to improve the future performance of working dogs. Although there is ample evidence that enrichment and socialization have a positive impact on adult behavior in dogs, there is no evidence ENS in and of itself has any lasting effect on dog behavior. Since the purported benefits are large and the required manipulations are minor, we sought: a) to evaluate the effects of ENS on self-confidence, motivation, and aggressive/defensive behavior in pups from 2 months of age until 12 months; and b) to determine whether ENS increased the probability of dogs being considered as suitable for further training as working dogs. We used a split-litter design where half of the pups received the ENS manipulations, and the other half were a control group that was simply held for the same amount of time required by the ENS manipulations. Our results indeed show that the ENS treated dogs are more likely to be accepted for such training than were the control pups but that differences in behavior only appeared at testing on months 10 and 12. We suggest two reasons for our results. First, immediately after the ENS manipulations, the ENS pups probably were a bit more socialized than the control pups. This resulted in the caregivers spending more time with the ENS pups which further increased the discrepancy in socialization between the ENS and control pups. Second, since the caregivers were aware of the ENS manipulation their expectations resulted in more positive interactions with the pups resulting in improved behavior; a phenomenon known as the Pygmalion effect.
... Moreover, studies of early vocal behavior in infants have shown that vocalizations differ significantly between typically developing infants and infants with or at risk for ASD. Infant siblings of children with ASD present significant delays on both expressive language and gestural communication (Garrido et al., 2017;Iverson & Wozniak, 2007), as well as a less mature syllable production (Dawson et al., 2000). In particular, infants and toddlers with or at risk for ASD show delayed acquisition of canonical babbling and produce lower rates of canonical babbling, as well as smaller consonant inventories (Patten et al., 2014;Paul et al., 2011;Warren et al., 2010). ...
In this review, we discuss the topic of intersubjectivity and its disruption in Autism Spectrum Disorder, both from a developmental and neuroscientific perspective. We present evidence of the impact of an early neurodevelopmental disorder on the blooming of intersubjective abilities. We propose the existence of a basic, pre-reflective social cognition that originates from the sensorimotor networks and is anchored to their teleological organization. We present neurophysiological evidence of its involvement in the direct understanding of three core elements of action: its category, its goal, and its dynamic contour. Finally, we discuss to which extent the disrupted development of brain neuroarchitecture and connectivity in Autism could also possibly impact on basic social cognition, thus prevent- ing fluid, preverbal alignment with the others.
... Jok je dojenčkovo najpomembnejše sredstvo komuniciranja, kadar je v stiski, in vedno pomeni klic na pomoč odraslemu, naj se nemudoma odzove, mu pomaga zadovoljiti osnovne potrebe in poskrbi zanj (Kompan Erzar in Poljanec 2009;Sunderland 2008;Zeifman 2001). Če ga odrasli dosledno tolaži in njegov jok obravnava resno, v njegovih možganih nastanejo zelo učinkoviti sistemi za obvladovanje stresa tudi kasneje v življenju (Dawson 2000v Sunderland 2008Gunnar 1989v Sunderland 2008. Dosledno odzivanje na dojenčkov jok pomeni dosledno odzivanje na potrebe otroka in zadovoljevanje le-teh. ...
... Psychological stress during pregnancy impacts behavioral and developmental outcomes in humans (13). Early personality development in the child, schizophrenia, and emotional disturbances in offspring are all associated with maternal stress (14)(15)(16)(17). ...
Full-text available
Background: Genetics and environment both are critical in autism spectrum disorder (ASD), but their interaction (G × E) is less understood. Numerous studies have shown higher incidence of stress exposures during pregnancies with children later diagnosed with ASD. However, many stress-exposed mothers have unaffected children. The serotonin transporter ( SERT ) gene affects stress reactivity. Two independent samples have shown that the association between maternal stress exposure and ASD is greatest with maternal presence of the SERT short (S)-allele (deletion in the promoter region). MicroRNAs play a regulatory role in the serotonergic pathway and in prenatal stress and are therefore potential mechanistic targets in this setting. Design/methods: We profiled microRNA expression in blood from mothers of children with ASD, with known stress exposure during pregnancy. Samples were divided into groups based on SERT genotypes (LL/LS/SS) and prenatal stress level (high/low). Results: Two thousand five hundred mature microRNAs were examined. The ANOVA analysis showed differential expression (DE) of 119 microRNAs; 90 were DE in high- vs. low-stress groups (stress-dependent). Two (miR-1224-5p, miR-331-3p) were recently reported by our group to exhibit stress-dependent expression in rodent brain samples from embryos exposed to prenatal stress. Another, miR-145-5p, is associated with maternal stress. Across SERT genotypes, with high stress exposure, 20 significantly DE microRNAs were detected, five were stress-dependent. These microRNAs may be candidates for stress × SERT genotype interactions. This is remarkable as these changes were from mothers several years after stress-exposed pregnancies. Conclusions: Our study provides evidence for epigenetic alterations in relation to a G × E model (prenatal maternal stress × SERT gene) in ASD.
... Although risk calculators have become a popular risk estimation tool in physical health domains, they have been under-utilized in mental health (Bernardini et al., 2017;Wakschlag et al., 2021). The mental health field could greatly benefit from this approach, given the robust support for the efficacy of prevention programs during early and/or vulnerable periods of development (Bernardini et al., 2017;Dawson, Ashman, & Carver, 2000;Luby et al., 2019). ...
The National Institute of Mental Health Research Domain Criteria’s (RDoC) has prompted a paradigm shift from categorical psychiatric disorders to considering multiple levels of vulnerability for probabilistic risk of disorder. However, the lack of neurodevelopmentally-based tools for clinical decision-making has limited RDoC’s real-world impact. Integration with developmental psychopathology principles and statistical methods actualize the clinical implementation of RDoC to inform neurodevelopmental risk. In this conceptual paper, we introduce the probabilistic mental health risk calculator as an innovation for such translation and lay out a research agenda for generating an RDoC- and developmentally-informed paradigm that could be applied to predict a range of developmental psychopathologies from early childhood to young adulthood. We discuss methods that weigh the incremental utility for prediction based on intensity and burden of assessment, the addition of developmental change patterns, considerations for assessing outcomes, and integrative data approaches. Throughout, we illustrate the risk calculator approach with different neurodevelopmental pathways and phenotypes. Finally, we discuss real-world implementation of these methods for improving early identification and prevention of developmental psychopathology. We propose that mental health risk calculators can build a needed bridge between RDoC’s multiple units of analysis and developmental science.
The period immediately after birth is a critical developmental window, capturing rapid maturation of brain structure and a child’s earliest experiences. Large-scale brain systems are present at delivery, but how these brain systems mature during this narrow window (i.e. first weeks of life) marked by heightened neuroplasticity remains uncharted. Using multivariate pattern classification techniques and functional connectivity magnetic resonance imaging, we detected robust differences in brain systems related to age in newborns (n = 262; R2 = 0.51). Development over the first month of life occurred brain-wide, but differed and was more pronounced in brain systems previously characterized as developing early (i.e. sensorimotor networks) than in those characterized as developing late (i.e. association networks). The cingulo-opercular network was the only exception to this organizing principle, illuminating its early role in brain development. This study represents a step towards a normative brain “growth curve” that could be used to identify atypical brain maturation in infancy.
The development of anxiety disorders is often linked to individuals’ negative experience. In many animals, development of anxiety‐like behavior is modeled by manipulating individuals’ exposure to environmental enrichment. We investigated whether environmental enrichment during early ontogenesis affects anxiety‐like behavior in larval zebrafish. Larvae were exposed from hatching to either an environment enriched with 3D‐objects of different color and shape or to a barren environment. Behavioral testing was conducted at different intervals during development (7, 14, and 21 days post‐fertilization, dpf). In a novel object exploration test, 7 dpf larvae of the two treatments displayed similar avoidance of the visual stimulus. However, at 14 and 21 dpf, larvae of the enriched environment showed less avoidance, indicating lower anxiety response. Likewise, larvae of the two treatments demonstrated comparable avoidance of a novel odor stimulus at 7 dpf, with a progressive reduction of anxiety behavior in the enriched treatment with development. In a control experiment, larvae treated before 7 dpf but tested at 14 dpf showed the effect of enrichment on anxiety, suggesting an early determination of the anxiety phenotype. This study confirms a general alteration of zebrafish anxiety‐like behavior due to a short enrichment period in first days of life.
When left untreated, perinatal mood and anxiety disorders (PMADs) are associated with increased risk for numerous adverse effects for the mother, the infant, and the mother-infant dyad. The significant risks of untreated symptoms must be weighed against the risks of treatment options in pregnancy and lactation. It is paramount that providers and patients understand the risk of not treating during pregnancy, as the symptoms themselves can lead to great harm. This chapter will review the correlated risks of untreated symptoms in detail, as well as the impact on lactation and breastfeeding. Lastly, the economic impact of untreated PMADs will be addressed.
C. H. Waddington's (1942) notion of canalization has been widely invoked in developmental psychology to conceptualize species-typical regularities in behavioral development as genetically determined. In contrast, a developmental systems view, such as the one described in the present article, sees the genes as only one component in a hierarchy of influences, all of which contribute to canalize behavioral development. A key issue is that genetic activity does not by itself produce finished traits; differentiation occurs as a consequence of events above as well as below the cellular level, necessarily involving factors in addition to genetic influences to canalize behavioral development. In exploring the possible experiential canalization of development, it was found that the mallard duck embryo's contact call plays a canalizing role in species-specific perceptual development (G. Gottlieb; see record 1991-11868-001 ). Thus, normally occurring experience, in concert with genetic and other activities, can canalize behavioral development. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The cAMP-responsive element-binding protein (CREB) has been implicated in the activation of protein synthesis required for long-term facilitation, a cellular model of memory in Aplysia. Our studies with fear conditioning and with the water maze show that mice with a targeted disruption of the alpha and delta isoforms of CREB are profoundly deficient in long-term memory. In contrast, short-term memory, lasting between 30 and 60 min, is normal. Consistent with models claiming a role for long-term potentiation (LTP) in memory, LTP in hippocampal slices from CREB mutants decayed to baseline 90 min after tetanic stimulation. However, paired-pulse facilitation and posttetanic potentiation are normal. These results implicate CREB-dependent transcription in mammalian long-term memory.
Behavior-state matching and synchrony in interactions were assessed in 48 depressed and nondepressed mother–infant dyads when the infants were 3 months old. Attentive/affective behavior states were coded for the infants and mothers on a negative to positive scale. The depressed mothers and their infants matched negative behavior states more often and positive behavior states less often than did the nondepressed dyads. The total percentage of time spent in matching behavior states was less for the depressed than for the nondepressed dyads. Cross-spectral analyses of the mothers' and the infants' behavior-state time series suggested only a trend for greater coherence or synchrony in the interactions of the nondepressed dyads. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
C. H. Waddington's (1942) notion of canalization has been widely invoked in developmental psychology to conceptualize species-typical regularities in behavioral development as genetically determined. In contrast, a developmental systems view, such as the one described in the present article, sees the genes as only one component in a hierarchy of influences, all of which contribute to canalize behavioral development. A key issue is that genetic activity does not by itself produce finished traits; differentiation occurs as a consequence of events above as well as below the cellular level, necessarily involving factors in addition to genetic influences to canalize behavioral development. In exploring the possible experiential canalization of development, it was found that the mallard duck embryo's contact call plays a canalizing role in species-specific perceptual development (G. Gottlieb; see record 1991-11868-001). Thus, normally occurring experience, in concert with genetic and other activities, can canalize behavioral development. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
Investigated the effects of maternal stress during pregnancy on object permanence (OP) performance in rhesus monkey infants. Beginning on Day 45 postpartum, 24 rhesus monkey infants were tested 4 times per week on a series of tests examining Piagetian OP. 12 Ss were the offspring of females exposed to a daily 10-min mild stressor during pregnancy, while 12 were born to mothers undisturbed during pregnancy. Prenatally stressed infants took longer to recover an object that was partially obstructed or observed to vanish. Results suggest a relationship between prenatal stress and subsequent cognitive impairment in rhesus monkey offspring. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The current study investigated the relationship between previous, recent, or chronic maternal depressive symptoms and subtypes of child behavior problems rated by teachers and mothers among 64 low-income children aged 4–6 years. Sixty-nine percent of mothers with high depressive symptom levels at the preschool assessment had also reported high symptom levels during the child's infancy. Children whose mothers reported depressive symptoms at both ages exhibited significantly elevated rates of hostile behavior problems in the classroom and at home compared to children of never-depressed mothers. Children of mothers who were previously but not currently depressed showed significantly more anxious and withdrawn behavior at school and at home, while children of recently depressed mothers were more hyperactive and demanding. Child cognitive scores and father absence were also related to behavior problems, but these variables did not mediate the independent effects of chronicity and timing of maternal depressive symptoms on the types of child symptoms displayed.