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Behavioral neuroscience spent much of the twentieth century seeking the fundamental rules of cerebral organization. One underlying assumption of much of that work was that there is constancy in cerebral organization and function, both between and within mammalian species (e.g., Kaas, 2006). One unexpected principle to emerge, however, was that although there is much constancy in cerebral functioning, there is remarkable variability as well. This variability reflects the brain's capacity to alter its structure and function in reaction to environmental diversity, thus reflecting a capacity that is often referred to as brain plasticity. Although this term is now commonly used in psychology and neuroscience, it is not easily defined and is used to refer to changes at many levels in the nervous system ranging from molecular events, such as changes in gene expression, to behavior (e.g., Shaw & McEachem, 2001). The relationship between molecular or cellular changes and behavior is by no means clear and is plagued by the problems inherent in inferring causation from correlation. Nonetheless, we believe that it is possible to identify some general principles of brain plasticity and behavior. As we do so we will attempt to link these principles to potential clinical implications. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
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Principles of neuroplasticity and behavior
Bryan Kolb and Robbin Gibb
Behavioral neuroscience spent much of the twentieth
century seeking the fundamental rules of cerebral
organisation. One underlying assumption of much
of that work was that there is constancy in cerebral
organisation and function, both between and within
mammalian species (e.g., Kaas, 2006). One unex-
pected principle to emerge, however, was that
although there is much constancy in cerebral func-
tioning, there is remarkable variability as well. This
variability reflects the brain’s capacity to alter its
structure and function in reaction to environmental
diversity, thus reflecting a capacity that is often
referred to as brain plasticity. Although this term is
now commonly used in psychology and neuro-
science, it is not easily defined and is used to refer to
changes at many levels in the nervous system ranging
from molecular events, such as changes in gene
expression, to behavior (e.g., Shaw & McEachern,
2001). The relationship between molecular or cellular
changes and behavior is by no means clear and is
plagued by the problems inherent in inferring causa-
tion from correlation. Nonetheless, we believe that it
is possible to identify some general principles of brain
plasticity and behavior. As we do so we will attempt to
link these principles to potential clinical implications.
Assumptions underlying brain plasticity
As we consider the principles of brain plasticity, we
need to consider five underlying assumptions that
will color our perspective.
Brain plasticity takes advantage of a basic,
but flexible, blueprint for cerebral organisation
that is formed during development
The process of brain development is a remarkable
feat of nature. Billions of neurons and glia must be
generated, they must migrate to their correct loca-
tions, and they must form neuronal networks that
can underlie functions that range from as simple as
postural reflexes to complex thought. Although a
complete genetic blueprint for neuronal organisa-
tion might be possible for a simple creature like the
nematode Caenorhabditis elegans, which has a total
of 302 neurons, it is not remotely possible for the
mammalian brain to have a specific blueprint (Katz,
2007). The best that nature can be expected to do is
to produce a rough blueprint of cerebral organisa-
tion that must be shaped by experience in order for
animals to exploit specific ecologies, including cul-
tures. The disadvantage of such flexibility is that it is
possible to make errors, but this problem is certainly
outweighed by the advantage of having a brain that
can learn complex motor or perceptual skills that
could scarcely have been anticipated by evolution
thousands or even millions of years before.
Cerebral functions are both localised
and distributed
One of the great issues in the history of brain
research relates to whether functions are discretely
localised in the brain (for a review, see Kolb &
Whishaw, 2001). The resolution to this debate was
important because the degree of localisation of
Cognitive Neurorehabilitation, Second Edition: Evidence and Application, ed. Donald T. Stuss, Gordon Winocur and
Ian H. Robertson. Published by Cambridge University Press. © Cambridge University Press 2008.
[6–21] 15.3.2008 1:02PM
function places constraints on the potential extent
of functional plasticity. The more distributed a
function, the greater the likelihood that the neural
networks underlying the function will be flexible
after a brain injury. As we enter the twenty-first
century it is clear that functions are at once localised
and distributed. Consider language. Although there
are discrete language zones in the cortex, language
is much more distributed across the cortex than
would have been expected from the classical neu-
rologists (e.g., Geschwind, 1972). But there are limits
to distributed functions, especially in the sensory
systems. For example, information coming to the
occipital lobe travels from the eye to subcortical
areas, then to Visual area 1 (V1) where it is pro-
cessed, and then is sent on to other visual regions
such as V2 and on to V3 etc. If V1 is only partially
damaged, V2 will still receive some input and can
function, albeit not normally. Further, after partial
damage, neural networks in V1 and V2 could reor-
ganise and possibly facilitate some type of func-
tional improvement. But if V1 is completely (or
substantially) damaged, downstream visual areas,
such as V2, will not be provided with appropriate
inputs and no amount of reorganisation in V2 could
instantiate functional recovery. The partial localisa-
tion of functions thus places significant constraints
upon plasticity and recovery of function.
Changes in the brain can be shown at many
levels of analysis
Although it is ultimately the activity of neuronal
networks that controls behavior, and thus changes
in neuronal network activity that are responsible for
behavioral change, there are many ways to examine
changes in the activity of networks. Changes may be
inferred from global measures of brain activity, such
as in the various forms of in vivo imaging, but such
changes are far removed from the molecular pro-
cesses that drive them. Changes in the activity of
networks likely reflect changes at the synapse but
changes in synaptic activity must result from more
molecular changes such as modifications in chan-
nels, gene expression, and so on. The problem in
studying brain plasticity is to choose a surrogate
marker that best suits the question being asked.
Changes in potassium channels may be perfect for
studying presynaptic changes at specific synapses
that might be related to simple learning in inverte-
brates (e.g., Kandel, 1979; Lukowiak et al., 2003;
Roberts & Glanzman, 2003) but are impractical for
understanding sex differences in language process-
ing. The latter might best be studied by in vivo
imaging or postmortem analysis of cell morphology
(e.g., Jacobs et al., 1993). Neither level of analysis is
“correct.” The appropriate level must be suited for
the research question at hand.
One convenient surrogate for synaptic change in
laboratory studies of brain and behavior is dendritic
morphology. In this type of study entire neurons are
stained with a heavy metal (gold, silver or mercury)
and the dendritic space is calculated (Figure 1.1). It
is assumed that by knowing the space available for
Figure 1.1. Example of a Golgi-Cox stained pyramidal cell
from layer III of the parietal cortex of th e rat. A. Higher
power magnification showing spines on an apical branch.
B. Higher power magnification showing spines on a basilar
branch. (Photograph courtesy of Grazyna Gorny.)
Principles of neuroplasticity and behavior 7
[6–21] 15.3.2008 1:02PM
synapses it is possible to infer associations between
synaptic organisation and behavior notwithstanding
the problems inherent in correlational studies dis-
cussed below. The studies of Jacobs and Scheibel
(Jacobs et al., 1993; Jacobs & Scheibel, 1993) provide
a good example. These researchers examined the
dendritic morphology of pyramidal neurons in post-
mortem brains of people whose educational and
employment history was known. Comparison of
synapse numbers in the posterior speech zone of
people with university education, high-school edu-
cation, or less than high-school education showed
that there were progressively more synapses on the
neurons from brains with more education. The
study cannot tell us why this correlation is present
but it tells us that there is some relationship
between experience and synaptic organisation.
To be functionally meaningful, changes
reflecting brain plasticity must persist for at
least a few days
Changes in neuronal activity related to brain plasti-
city may be of limited duration, perhaps in the order
of seconds or milliseconds. While such changes are
interesting in their own right, we are focusing our
attention on longer-lasting changes that persist for
at least a few days. This is a practical assumption as
we think about how experiences might be related to
chronic behavioral changes seen after brain injury
or with addiction.
Correlation is not a four-letter word
By its very nature, behavioral neuroscience searches
for neuronal correlates of behavior. Some of these
changes are directly associated with behavior but
others are more ambiguous. Consider an example.
If an individual is given a psychoactive drug we may
see an obvious acute behavioral change such as
increased motor activity. If the drug is taken repeat-
edly, we may see that there is an escalating increase
in the drug-dependent hyperactivity, a phenom-
enon referred to as drug-induced behavioral sensiti-
sation. If we were to look for changes in the brain
that were related to the observed sensitisation we
might find a change in synapse number in some
discrete brain region such as the nucleus accum-
bens (NAcc). Both the behavioral change and the
synaptic change are correlates of the drug adminis-
tration. But what is the relationship between the
behavioral and synaptic change? We can conclude
that the drug caused the behavioral change but it is
less clear that the drug directly caused the neuronal
change. Perhaps the behavioral change caused the
neuronal change or maybe both were related to
some other change in the brain. Thus, a common
criticism of studies trying to link neuronal changes
to behavior is that “they are only correlates.” This is
true but it is hardly a reason to dismiss such studies.
The task is to try to break the correlation by showing
that one change can occur without the other. The
presence of such evidence would disconfirm cau-
sality but, unfortunat ely, the failure to break the
correlation is not proof of causation. Ultimately
the proof would be in showing how the synaptic
changes arose, which would presumably involve
molecular analysis such as a change in gene tran-
scription. For many studies this would be an
extremely difficult challenge and often impractical.
It is our view that once we understand the “rules”
that govern neuronal and behavioral change, we will
be better able to look for molecular changes.
Furthermore, we argue that a certain level of ambi-
guity in the degree of causation is perfectly justifi-
able at this stage of our knowledge. Understanding
the precise mechanism whereby the synaptic
changes might occur is not necessary to proceed
with further studies aimed at improving functional
Principles of brain plasticity
Although it is presumptuous to try to identify basic
principles of brain plasticity when so much is still
unknown, we believe that the progress over the past
decade allows us to begin to identify some of the
rules underlying brain plasticity. These principles
should be seen as a work in progress that will
8 Bryan Kolb and Robbin Gibb
[6–21] 15.3.2008 1:02PM
undoubtedly be expanded and further demonstra-
ted over the next decade.
When the brain changes, this is reflected in
behavioral change
The primary function of the brain is to produce
behavior but behavior is not constant. We learn
and remember, we create new thoughts or images,
and we change throughout our lifetime. All of these
processes require changes in neural networks. It
follows that whenever neural networks change,
behavior, including mental behavior, will also
change. A corollary of this principle is that in order
to change behavior we must change the brain. This
latter idea is especially important as we search for
treatments for brain injuries or diseases.
Plasticity is found in all nervous systems and
the principles are conserved
Even the simplest animals, such as the nematode
C. elegans, can show simple learning that is corre-
lated with neuronal plasticity (e.g., Rose & Rankin,
2001). Similarly, there is now an extensive literature
showing neuronal and other changes in invertebrates
such assea snailAplysia during simplelearning, inclu-
ding associative learning. Furthermore, it now has
become clear that both simple and complex nervous
systems show both pre- and postsynaptic changes
and that the changes are remarkably similar (e.g.,
Rose & Rankin, 2001). There is reason to believe,
for example, that there are NMDA-like changes in
learning in both mammals and invertebrates (e.g.,
Roberts & Glanzman, 2003). The details of the postsy-
naptic second messengers may differ in simple and
complex systems but the general principles appear to
be conserved across both simple and complex animals.
The brain is altered by a wide range
of experiences
Virtually every experience has the potential to alter
the brain, at least briefly. It now has been shown
that a wide variety of experiences can also produce
enduring changes, ranging from general sensory-
motor experience to psychoactive drugs to electrical
brain stimulation (see Table 1.1). The bulk of these
studies have used morphological techniques such
as electron microscopy or Golgi-like stains and have
shown that experience-dependent changes can be
seen in every species of animals tested, ranging
from fruit flies and bees to rats, cats and monkeys
(for a review see Kolb & Whishaw, 1998). Consider a
few examples.
When animals are placed in complex environ-
ments rather than simple laboratory cages, within
30 days there is about a 5% increase in brain weight
and cortical thickness, an increase in cortical ace-
tylcholine and neurotrophic factors (e.g., nerve
growth factor (NGF), brain-derived neurotrophic
factor (BDNF), fibroblast growth factor-2 (FGF-2)),
as well as changes in physiological properties of
neurons such as those measured in studies of
Table 1.1. Factors affecting the synaptic organisation
of the normal brain
Sensory and motor experience
Greenough & Chang,
Task learning Greenough & Chang,
Gonadal hormones and stress
Stewart & Kolb, 1988
Psychoactive drugs (e.g.,
stimulants, THC)
Robinson & Kolb,
Neurotrophic factors (e.g., NGF,
Kolb et al., 1997
Natural rewards (e.g., social
interaction, sex)
Fiorino & Kolb, 2003
Ageing Kramer et al., 2004
Stress McEwen, 2005
Anti-inflammatories (e.g., COX-2
Silasi & Kolb, 2007
Diet (e.g., choline) Meck & Williams,
Electrical stimulation: kindling Teskey et al., 2001
LTP Ivanco et al., 2000
Direct cortical stimulation Teskey et al., 2004
Principles of neuroplasticity and behavior 9
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long-term potentiation (LTP) (for a review see Kolb
& Whishaw, 1998). Although most studies have
focused on neocortical changes, similar changes
can also be seen in hippocampus and striatum
(e.g., Comery et al., 1996; Juraska, 1990). The ana-
tomical and physiological changes are associated
with improved performance on tests of both motor
and cognitive behaviors and although the data are
correlational, it is generally assumed that the mor-
phological changes are responsible for the facilita-
tion in behavior.
Experience-dependent changes in the brain do
not require procedures as intense as complex hous-
ing, however. Increased social experience selec-
tively increases synapses in the orbital frontal
cortex (Fiorino & Kolb, 2003; Hamilton et al., 2003).
We have also seen that tactile stimulation either in
infancy or adulthood alters cells in sensorimotor
cortex (e.g., Gibb & Kolb, submitted a,b). This latter
treatment has also been used in animals with cort-
ical injuries to stimulate dendritic growth and facil-
itate functional recovery. Although there is little
evidence that exercise can enhance plasticity in
the normal brain, there is growing evidence that it
can facilitate plastic changes in the injured lab ani-
mal and human brain (e.g., Gibb et al., 2005; Kramer
et al., 2006).
A final example can be seen in the effects of psy-
choactive drugs. Robinson & Kolb (1999a) showed
that repeated doses of amphetamine or cocaine
given to rats produced a persisting increase in den-
dritic length and spine density localised to the
medial prefrontal cortex (mPFC) and NAcc but not
to adjacent sensorimotor cortical regions. It now
appears that repeated doses of all psychoactive
drugs, including prescription drugs, change neuro-
nal morphology. The details of drug-induced mor-
phological changes vary with the drug but the
general principle is that psychoactive drugs alter
neuronal morphology in the cerebrum and this
can be seen both in dendritic measures as well as
in a variety of more molecular measures (for a
review, see Hyman et al., 2006). Once again, the
relationship between the behavioral changes, such
as drug-induced behavioral sensitisation, and the
altered neuronal networks has yet to be proven but
there is little doubt that the chronic effects of drug
use are not neutral to cerebral functioning. The
ability of drugs to alter neuronal morphology may
be important for rehabilitation because drugs can
be combined with behavioral treatments such as
rehabilitation therapy, including cognitive therapy
(e.g., Gonzalez et al., 2006).
Taken together the examples described above
illustrate the power of experience in modulating
cerebral networks and in facilitating remodeling
stimulated by behavioral therapies. Although expe-
rience is likely more effective in remodeling neural
networks as they are repairing after injury, improve-
ment still can occur late after injury (e.g., Hodics
et al., 2006). Psychomotor stimulants may provide a
powerful way of reinstigating cerebral plasticity late
after injury to facilitate the effectiveness of behav-
ioral therapies.
Plastic changes are age-specific
When weanling, adult, or senescent rats were placed
in a complex environment, we had anticipated that
we would find larger changes in the younger ani-
mals but to our surprise, we found a qualitative
difference in the neuronal response to the same
experience. Thus, whereas rats at all ages showed
an increase in dendritic length and branching in
neocortical pyramidal cells after complex housing,
rats placed in the environments as infants showed a
decrease in spine density whereas young adult or
senescent rats showed an increase in spine density
(Kolb et al., 2003a). A similar drop in spine density
was found in later studies in which newborn rats
were given tactile stimulation with a soft brush for
15 min, three times daily over the first 10 days of life
(Kolb & Gibb, submitted).
The obvious question is whether the behavioral
effects to the complex housing are the same
depending upon the age at experience. Our early
results suggest that there is an advantage in both
cognitive and motor tasks and that it does not mat-
ter when the experience occurred. There are clearly
different ways to organise neuronal networks to
10 Bryan Kolb and Robbin Gibb
[6–21] 15.3.2008 1:02PM
enhance both motor and cognitive behaviors. This
point is important as we consider treatments for
brain dysfunction there may be many ways to
facilitate recovery.
Early events, including prenatal events, can
influence the brain throughout life
Our finding that early postnatal experiences could
alter neuronal organisation led us to ask if prenatal
experiences might also alter cerebral organisation.
In one study pregnant dams were placed in complex
environments for 8 hours a day prior to their preg-
nancy and then throughout the 3 week gestation. (In
different studies the dams were in the environments
during the day or night but it made no difference.)
Analysis of the adult brains of their infants showed a
decrease in dendritic length and an increase in spine
density in adulthood (Gibb et al., submitted). We
were surprised both that there was a large effect of
prenatal experience and that it was qualitatively
different than experience either in the juvenile
period or in adulthood. More recently we have
shown that a variety of prenatal experiences alter
brain organisation in adulthood including prenatal
tactile stimulation (i.e., stimulation of the pregnant
dam), exercise during pregnancy, prenatal stress
and psychoactive drugs. All of these experiences
also chronically alter motor and cognitive functions,
with the precise effect varying with the different
experiences (for a review see Kolb et al., in press).
Although we do not know how these prenatal
changes might influence the effect of postnatal
experiences, it is clear that prenatal experiences
produce chronic effects on brain organisation and
behavior. One is reminded here of the idea of cog-
nitive (or neural) reserve as being key factors in the
onset of dementias (e.g., Stern, 2006). Might early
life events influence cognitive reserve in adulthood
or senescence?
Plastic changes are area dependent
Although we are tempted to expect plastic changes in
neuronal networks to be fairly general, it is becoming
clear that many experience-dependent changes are
highly specific. The clearest examples can be seen in
neuropsychological studies in which animals are
trained on cognitive or motor tasks. For example,
rats trained on a visuospatial task show specific
changes in visual cortex whereas rats trained on
motor tasks show specific changes in motor cortex
(e.g., Greenough & Chang, 1989; Kolb & Cioe, sub-
mitted; Withers & Greenough, 1989). Such task-
dependent specific changes are reasonable in view
of the relative localisation of functions in the cortex.
But not all area-dependent changes are so easily
predicted. Consider two examples.
We noted above that the effect of psychoactive
drugs appeared to be selective to regions that
receive dopaminergic innervation. We therefore
were surprised to find that the orbitofrontal cortex
(OFC), another region that receives dopaminergic
innervation, showed drug-induced changes that are
opposite to those in mPFC and NAcc (Robinson &
Kolb, 2004). Thus, whereas psychomotor stimulants
increased dendritic length and spine density in the
mPFC, they decreased the same measures in
the OFC. The contrasting effects of these drugs on
the two prefrontal regions are puzzling given the
similarity in thalamic and other connections of the
two regions (e.g., Uylings et al., 2003). Curiously,
there also are differential effects of gonadal hor-
mones on the two prefrontal regions as well: mPFC
neurons have more synaptic space in males whereas
OFC neurons have more space in females (Kolb &
Stewart, 1991). Although we do not yet know what
such differences mean behaviorally, there can be
little doubt that the differential response of two
such similar cortical regions to drugs and hormones
must be important in understanding their functions.
Plastic changes are time-dependent
There is growing evidence that plastic changes are
not constant and can change over time. The clearest
example comes from drug studies. For example,
although there are large increases in spine density
and dendritic length 2 weeks after cessation of cocaine
administration, these changes slowly disappear over a
Principles of neuroplasticity and behavior 11
[6–21] 15.3.2008 1:02PM
4-month period (Kolb et al., 2003b). In contrast,
when rats are given morphine and the brains are
examined immediately after drug cessation, there
is an increase in dendritic arborisation in NAcc
ez et al., 2006) but a month later
the changes are just the opposite (Robinson & Kolb,
1999b). One reason for the time-dependent effects
of the drug exposure may be that behavior is chang-
ing as the animals are first in withdrawal and then
adapt to the drug’s absence.
Time-dependent plasticity also can be seen in
response to repeated electrical brain stimulation.
Repeated low intensity stimulation can slowly lead
to the development of spontaneous seizures, a phe-
nomenon known as kindling (Teskey, 2001). The
development of seizures is correlated with changes
in dendritic length and spine density that normalise a
month after cessation of electrical stimulation
(Teskey et al., 2001). Curiously, the stimulation also
produces physiological changes that do not change.
In this case it appears that the experience (i.e., the
electrical stimulation) produces both dendritic and
physiological change but the two are not related.
The possibility that there are different chronic
and transient experience-dependent changes in
cerebral neurons is consistent with genetic studies
showing that there are different genes expressed
acutely and chronically in response to complex
environments (Rampon et al., 2000). The difference
in how transient and persistent changes in neuronal
networks relate to behavior is unknown.
Brain injury produces plastic changes
that vary with etiology
Although we may be able to point to a specific prox-
imal cause of a brain injury, such as a stroke, the end
result of brain injury is not the result of a single
causative event. Rather, there is an initial event fol-
lowed by a cascade of cellular events that can seri-
ously compromise the injured brain as well as brain
regions that were not directly injured. Such post-
injury changes may be rapid, such as changes in pH
or ionic balance that can occur within seconds or
minutes after an injury, or they may be slower such
as the production of glia that migrate to the injured
tissue. Of more interest, however, are the longer-
term changes in neuronal networks that underlie
the emerging post-injury functions. The nature of
these changes varies with the cause of the injury.
The adult brain can be injured in numerous ways,
including especially stroke, head trauma, and neu-
rosurgical excision for disease. The literature on
functional recovery and rehabilitation quite reason-
ably has assumed that after the initial post-injury
period, patients with different types of brain injuries
are likely to benefit similarly from treatments.
However, this presumption rests on the assumption
that the reparative processes that spontaneously
begin after injury are similar for different types of
injuries. A study by Gonzalez & Kolb (2003) leads us
to question this assumption.
These authors gave rats equivalent lesions of the
sensorimotor cortex but produced the damage
either by arterial occlusion, vascular stripping, or
surgical suction. The behavioral outcomes were
similar in three groups, with severe chronic motor
symptoms in the contralateral limbs. Similarly, the
infarct volumes were essentially identical across the
groups. What was surprising, however, was when
the authors examined the morphology of neurons
in the striatum and perilesional area they found that
each group was different (see also Szele et al., 1995).
For instance, the brains with suction lesions showed
atrophy of dendritic fields, whereas the brains of
animals with vascular stripping lesions showed
reconfigured fields with increased dendritic arbor-
isation. We hasten to note, however, that the behav-
ioral recovery within the different groups was
comparable, at least with the behavioral measures
that the authors employed. This finding is reminis-
cent of the evidence showing that perinatal experi-
ences can have different effects on brain organisation
but similar effects on behavior.
One message from the Gonzalez and Kolb study is
that capacity for treatment-induced recovery is
likely not equivalent after injuries with differing
etiologies because the brain is changing differently
with different etiologies. This conclusion has obvious
implications for rehabilitation of human patients
12 Bryan Kolb and Robbin Gibb
[6–21] 15.3.2008 1:02PM
although we unaware of any direct studies on
this issue.
Neuronal plasticity following brain injury
varies with age
It has been known since the time of Broca that
children seem to have a better outcome after early
injury than adults, but we are just beginning to
understand why this might be so. The first system-
atic studies on the comparative effects of early brain
injury were done by Margaret Kennard, who studied
the effects of motor cortex lesions in infant mon-
keys. Her seminal observation was that the animals
with early lesions showed better recovery of motor
functions than those with injuries in adulthood
(e.g., Kennard, 1942). Although there was later sup-
port for the Kennard findings that “earlier is better”
(e.g., Akert et al., 1960), other studies in monkeys
were less supportive (Goldman, 1974). It was not
until age was systematically varied in studies in
rats and cats that the relationship between age at
injury and functional outcome became clearer.
We have examined the behavior of adult rats that
had focal injuries to the mPFC, motor, temporal,
posterior parietal, or posterior cingulate cortex at
postnatal days 1, 4, 7, 10, or 90 (i.e., adult). The
overall result was that regardless of the location of
injury, the functional outcome was always best after
injury during the second week of life, which in the
rat is a time of intense cerebral synaptogenesis and
glial formation. A similar pattern of results can be
seen in parallel studies of the effects of cortical
lesions in kittens by Villablanca and his colleagues
(e.g., Schmanke & Villablanca, 2001; Villablanca
et al., 1993), although because the rat and cat
develop at different rates the precise ages are differ-
ent in the two species. The key point here is that
birth date is irrelevant it is the stage of neural
development that is important.
But what brain changes account for the age effects?
In principle, there are three ways that an injured
brain could compensate for lost tissue: (1) reorgan-
isation of existing neuronal networks; (2) develop-
ment of novel networks; and (3) regeneration of the
lost tissue. All three occur after early brain injury.
We consider each briefly.
The first studies on anatomical compensations
after early brain injury focused on connectivity
after unilateral damage to the motor system (e.g.,
Castro, 1990; D’Amato & Hicks, 1980; Villablanca &
Gomez-Pinilla, 1987; Whishaw & Kolb, 1988). The
general finding was that if there is perinatal damage
to the cortex that normally gives rise to the cortico-
bulbar and corticospinal pathways, the intact path-
way on the opposite side sprouts new connections
both to subcortical motor regions of the damaged
hemisphere as well as through an enlarged ipsilat-
eral corticospinal pathway. These new pathways are
believed to underlie the better motor outcomes of
the early injuries. Parallel findings are seen in the
sensory systems as novel pathways develop after
damage to primary visual cortex (see a review by
Payne & Lomber, 2001). Curiously, however, novel
pathways are not always beneficial. We have found
that damage to the mPFC in the first week of life
results in many anomalous networks but this is
correlated with poor outcome on various measures
of cognitive function (Kolb et al., 1994). In general,
however, the development of novel networks pro-
vides one explanation for the Kennard effect.
Another way to make inferences about neuronal
network remodeling is to examine dendritic morphol-
ogy after early injuries. The overall result of these
studies is that when functional outcome is good,
there is an increase in dendritic arborisation and
spine density in pyramidal neurons in the remaining
cortical mantle (e.g., Kolb et al., 1992, 1994; Kolb &
Whishaw, 1989). In contrast, when functional out-
come i s poor, there is an atrophy of dendritic arbor
and spine density. The emergence of the beneficial
compensatory changes in dendritic organisation takes
several weeks and is correlated with an emergence of
the improved cognitive function (Kolb & Gibb, 1993).
The idea that the generation of new tissue might be
possible after cerebral injury in postnatal mammals
was slow to develop and faced considerable skepti-
cism (e.g., Altman, 1962). There now is compelling
evidence that new neurons can be formed after
injury (see Chapter 22 by Stickland, Weiss, & Kolb,
Principles of neuroplasticity and behavior 13
[6–21] 15.3.2008 1:02PM
this volume) and especially after neonatal injury
(Kolb et al., 1998). For example, rats with mPFC
lesions around postnatal day 10 show a spontane-
ous regeneration of much of the lost tissue. Removal
of the tissue removes the functional recovery and
blockade of the tissue regrowth prevents the recov-
ery (e.g., Dallison & Kolb, 2003; Kolb et al., 1998).
Although the spontaneous regeneration can occur
after mPFC lesions such regeneration is uncom-
mon, but it can be induced by infusion of FGF-2
after cortical injury on day 10 (e.g., Monfils et al.,
2006). Again in these studies the removal of the new
tissue leads to a return of the functional deficits and
prevention of the regrowth prevents the functional
The effect of age on post-injury plasticity is likely
not only relevant during development. Teuber
(1975) reported that brain-injured soldiers also
showed a benefit of being younger: 18-year-olds
fared better than 25-year-olds who fared better
than older soldiers. It is generally assumed that
plastic changes are less likely to occur as the brain
ages but this has not been well studied and there is
little doubt that even senescent animals can show
considerable cortical plasticity (e.g., Kolb et al.,
2003a; Kramer et al., 2004). There still needs to be
systematic studies of cerebral plasticity and behav-
ior throughout the lifespan in both normal and
brain-injured animals.
Experience-dependent changes interact
As animals travel through life they have an almost
infinite number of experiences that could alter brain
organisation. There are virtually no experimental
studies attempting to determine how a lifetime’s
experiences might interact. We attempted to
address this question in a series of studies in which
animals received psychoactive drugs before place-
ment in complex environments (Hamilton & Kolb,
2005; Kolb et al., 2003b; Li et al., 2005). We hypoth-
esised that because the mPFC and NAcc were so
profoundly altered by the drugs, they might show
less (or no) change in response to the housing expe-
rience. To our surprise, not only did the mPFC and
NAcc show no response to the experience, but nei-
ther did any other cortical regions. For example,
pyramidal neurons in the parietal cortex, which
normally show large experience-dependent change
but little drug-dependent change, showed no
response to the complex housing after prior experi-
ence with amphetamine, cocaine, or nicotine. An
obvious question was whether prior experience
with complex housing would interfere with drug-
dependent changes. It does. Animals given complex
housing experience prior to repeated doses of nic-
otine show a much attenuated response to the drug.
Another example of interactions in experience-
dependent changes can be seen in the sexually
dimorphic response of cortical and hippocampal
neurons to complex housing. Juraska (1990) has
shown that whereas occipital cortex neurons show
increased dendritic arbor in response to complex
housing in males, there are no such changes in
females. In contrast, females show increased den-
dritic arbor in hippocampus whereas males do not.
One of the most common experiences of everyday
life is stress. In view of the significant effects of stress
on dendritic morphology and neurogenesis (see
Chapter 4 by Hunter & McEwen, this volume) it
seems likely that stress will interact with other
experience-dependent changes. We have found,
for example, that prenatal stress will block the nor-
mal recovery from cortical injury in the second week
of life (Gibb & Kolb, unpublished).
Finally, we note that prenatal exposure to experi-
ences described above interact with later postnatal
brain injury to produce differential changes in neuro-
nal networks and correlated functional recovery. For
instance, rats given prenatal experience via their
mother’s exposure to tactile stimulation or complex
housing show an attenuated effect of the later expe-
rience to perinatal brain injury and in some instances
show almost complete recovery that is correlated
with enhanced dendritic changes (Gibb et al., sub-
mitted). In contrast, rats exposed to stress or fluoxe-
tine prenatally show an exaggerated behavioral effect
of the same perinatal brain injuries and the poor
outcome is correlated with an apparent blockade of
post-injury compensatory changes (Day et al., 2003).
14 Bryan Kolb and Robbin Gibb
[6–21] 15.3.2008 1:02PM
Experience differentially affects the normal
and injured brain
We initially assumed that a given experience would
produce similar changes in the normal and injured
brain although there might be quantitative differen-
ces in the two conditions. It is now becoming clear
that the same experience can sometimes have the
opposite effect in the normal and injured brain.
One example is tactile stimulation during infancy:
there is a decrease in spine density in otherwise
normal animals but an increase in cortically injured
animals (Kolb & Gibb, submitted). Preliminary stud-
ies show similar paradoxically different effects of
other treatments such as complex housing and psy-
choactive drugs. This type of finding has important
implications for the development of rehabilitative
treatments so we need to understand why the effects
are different in the normal and injured brain.
Understanding normal plasticity gives us a key
to fixing the abnormal brain
It is our working hypothesis that as we learn more
about how the normal brain can be changed by
experience we will be able to apply this knowledge
to the injured brain. This strategy is proving to be
successful and Tables 1.2 and 1.3 summarise exam-
ples of developing treatments for damage to adult
and infant brains, respectively. The general conclu-
sion from this literature is that many, but not all,
factors that produce dendritic reorganisation and
functional benefit in the normal brain can provide
benefit after brain injury in both adults and infants.
The greatest benefit to lab animals with injury at
any age is clearly complex housing. As noted earlier,
complex housing leads to increases in various
growth factors, and includes social stimulation, sen-
sory stimulation, and increased motor activity. It is
likely the combination of all of these factors that
provides the large benefit. A key feature too is that
there is 24 hours of stimulation 7 days a week, rather
than an hour or so twice a week as might be more
likely with typical therapy given to human brain-
injured patients. Although it would be ideal to
provide human patients with some type of equiva-
lent therapy this would likely be impractical for
most health-care systems to provide. Furthermore,
placing animals or human patients with severe
motor deficits in complex environments is likely to
be quite stressful so we need to look at alternate
treatments. To date, the most promising treatments
include the use of psychomotor stimulants such as
amphetamine (Sutton et al., 1989) or nicotine
(Gonzalez et al., 2006). Clinical trials with amphet-
amine have given uneven results, likely because of
differences in lesion size. Laboratory studies suggest
that whereas rats with small lesions show a signifi-
cant benefit of amphetamine, those with large
Table 1.2. Factors enhancing recovery of the injured
adult brain
Complex housing
Biernaskie & Corbett, 2001
Olfactory stimulation Gonzalez & Kolb, 2006
Psychoactive drugs (e.g.,
Sutton et al., 1989
Neurotrophic factors (e.g.,
nerve growth factor)
Kolb et al., 1997
Anti-inflammatories (e.g.,
COX-2 inhibitors)
Silasi & Kolb, 2007
Electrical stimulation Teskey et al., 2004
Inosine Chen et al., 2002
Antibodies to No-Go Papadopoulos et al., 2006
Table 1.3. Factors enhancing recovery from early injury
Postinjury complex housing
Kolb & Elliott, 1987
Postinjury tactile stimulation Gibb & Kolb, submitted b
Prenatal complex housing Gibb et al., submitted
Prenatal tactile stimulation Gibb & Kolb, submitted a
Gonadal hormones Kolb & Stewart, 1995
Neurotrophic factors (e.g.,
fibroblast growth factor-2)
Comeau et al., 2007
Diet (e.g., choline; vitamins/
Halliwell et al., submitted
Olfactory stimulation Gonzalez & Kolb, 2006
Principles of neuroplasticity and behavior 15
[6–21] 15.3.2008 1:02PM
lesions do not (Goldstein & Davis, 1990). Nicotine
may prove to be more effective as it has wider-
spread changes in neuronal morphology in the nor-
mal brain and preliminary laboratory studies do
show that nicotine is much more effective than
amphetamine in treating animals with large cortical
strokes (Moroz & Kolb, 2005).
One additional treatment that is proving to be
effective in treating both laboratory animals and
stroke patients is direct cortical electrical stimula-
tion (Kleim et al., 2003; Teskey et al., 2003). An
obvious extension of the electrical stimulation stud-
ies is the combination of the stimulation with other
factors such as sensory or motor therapies or psy-
chomotor stimulation, although to our knowledge
this has not yet been tried. We note too that pre-
injury experiences may interact with post-injury
treatments. Recall the complex interactions of experi-
ence and dr ugs discussed above. In one preliminary
study we did show that prior exposure to nicotine
blocked the effectiveness of post-injury nicotine treat-
ment, a result reminiscent of the drug/environment
studies (Gonzalez & Kolb, unpublished observations).
In sum, we believe that there is considerable
potential in treating brain injury with factors that
are known to enhance brain plasticity in the normal
animal. It is likely that combinations of treatments
will prove the most effective. We do note too, how-
ever, that it is quite likely that injuries of different
etiologies will respond differently to specific factors.
The relative strength (and duration)
of plasticity is related to relevance of the
event to the animal and the intensity or
frequency of the events
Although most experiences must be repeated for us
to learn, some experiences need only be encountered
once and there is long-term change in behavior.
One example is food aversions that are related to a
single incidence of illness, a phenomenon referred
to as taste aversion conditioning. If animals are pre-
sented with a novel taste that is paired with illness,
there is an immediate and permanent aversion to
the taste. This learning requires only a single trial.
The key point is that food-related illness is highly
relevant to the animal and the brain is clearly pre-
pared to make certain associations (Yamamoto
et al., 1994). A parallel example can be seen in
imprinting in fowl (e.g., Lorenz, 1970), which is a
process where an organism learns, during a sensi-
tive period, to restrict its social preferences to a class
of objects. Horn and his colleagues have shown that
there are immediate changes in a part of the chick’s
hyperstriatum after visual imprinting. A variety of
rapidly occurring changes have been demonstrated
including an increase in dendritic length but a
decrease in spine density, increased glutamatergic
excitatory transmission, increased NMDA receptor
density, increased immediate early gene expression,
and other postsynaptic molecular changes (e.g.,
Horn 1998; Horn et al., 2001; Solomonia et al.,
2005). An important feature of the Horn experi-
ments is that although the most effective stimuli
for the changes are fowl, in the absence of fowl
there are still changes, thus suggesting flexibility in
the innate imprinting system.
The intensity of stimuli can be manipulated in
other models by varying drug doses, time in com-
plex housing, duration of electrical stimulation, etc.
For example, drug studies show that low doses of
psychomotor stimulants produce more restricted
changes in dendritic arborisation than higher
doses (e.g., Diaz-Heijtz et al., 2003) whereas addi-
tional doses of psychomotor stimulants produce
escalating increases in spine density (Kolb et al.,
2003b). Similarly, although animals may show
increased dendritic material in cortical pyramidal
cells after only a few days of complex housing, the
increases are much larger after longer durations
(e.g., Greenough & Chang, 1989).
One interesting aspect of electrical stimulation is
that whereas high frequency (25–200 Hz) stimulation
will produce enhanced postsynaptic potentiation
(i.e., long-term potentiation), low frequency stimula-
tion (3 Hz) will produce reduced potentiation (e.g.,
Cain, 2001; Teyler, 2001). The different forms of
stimulation lead to the activation of different post-
synaptic signaling pathways and a host of different
plastic changes (e.g., Teyler, 2001).
16 Bryan Kolb and Robbin Gibb
[6–21] 15.3.2008 1:02PM
Finally, a recent meta-analysis of physiotherapy
after stroke has concluded that the duration and
intensity of post-stroke therapy has a direct effect
on recovery on tests of daily living (Kwakkel et al.,
2004). These studies had no measure of brain
changes but the behavioral benefits of the therapy
provide a fairly strong suggestion that the treatment
did alter cerebral organisation.
Brain plasticity is not always a good thing
To this point we mostly have emphasised the plastic
changes in the brain that can support improved
motor and cognitive function. But plastic changes
can also interfere with behavior. For example, it is
reasonable to propose that some of the maladaptive
behavior of drug addicts could result from drug-
related changes in prefrontal neuronal morphology
(Robinson & Kolb, 2004). Another example can be
seen in schizophrenia.
Schizophrenia is a developmental disorder in
which the brain begins to show abnormalities in
morphology and behavior in late adolescence. The
abnormalities include reduced volumes of the fron-
tal and temporal lobes as well as increased ventric-
ular volume. Morphological analysis of neurons in
the prefrontal cortex of postmortem brains of schiz-
ophrenic patients shows a reduction in dendritic
arborization and spine density (Black et al., 2004).
The cause of these changes is poorly understood but
one hypothesis is that the changes are in response to
some developmental abnormality in the hippo-
campus (Lipska & Weinberger, 2002). Analysis of
hippocampal neurons in postmortem tissue from
schizophrenics shows disorganised organisation of
pyramidal cells that could result from some sort of
brain perturbation or genetic abnormality (Conrad
et al., 1991). The precise cause is difficult to study
in human postmortem tissue but it is possible to
manipulate the hippocampus in developing labora-
tory animals. Behavioral studies of laboratory ani-
mals with small ventral hippocampal lesions (or
hippocampal inactivation) in infancy show adult
functional disorders that are reminiscent of animals
with adult prefrontal injury (Lipska & Weinberger,
2002). Anatomical studies of similar animals show
reduced dendritic arborisation and spine density
similar to what has been seen in human schizo-
phrenic patients (Flores et al., 2005). Such changes
are not seen in rats with similar injuries in adult-
hood. It thus appears that both the behavioral and
morphological effects of the small ventral hippo-
campal injury only occur after a perturbation in
infancy. This perturbation is proposed to lead to
plastic changes in the developing prefrontal cortex
that lead to behavioral abnormalities in adulthood.
One prediction of this model is that the structural
abnormalities in the frontal lobe should not pro-
gress in adulthood but likely would remain static.
This appears to be the case (Pantelis et al., 2005).
There are many other examples of pathological
plasticity including pathological pain (Baranauskas,
2001), pathological response to sickness (Raison
et al., 2006), epilepsy (Teskey, 2001), and dementia
(Mattson et al., 2001). One goal is to find ways to
block or reverse pathological plasticity, although
this is likely to prove difficult.
We have tried to identify a set of principles that
describe the “rules” that define experience-dependent
changes in brain and behavior. Our choice of liter-
ature used to define the principles is obviously
biased and somewhat arbitrary but we believe that
we have provided a framework that others may find
useful in designing treatments for motor and cogni-
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Principles of neuroplasticity and behavior 21
... Neuroplasticity refers to the long-lasting changes in a brain's structure and function as a result of environmental input (Demarin et al., 2014;Kolb & Gibb, 2008). It is evident in non-speech motor learning (e.g., Doyon, 2008;Doyon et al., 2018) and speech-language learning (for a review, see Whelan et al., 2021). ...
... Brain changes related to neuroplasticity can occur throughout life during times of rapid synaptic development (Joja, 2013). They are more related to the stage of neural development than the specific chronological age of the individual (Kolb & Gibb, 2008). Nevertheless, greater therapeutic gains are made with infants and toddlers than neurologically mature individuals (Bruder, 2010;Grafman, 2000;Zwaigenbaum et al., 2013), possibly due to reorganization of existing neuronal networks or the development of novel synaptic networks during rapid neurological growth in young neurological systems (Kolb & Gibb, 2008). ...
... They are more related to the stage of neural development than the specific chronological age of the individual (Kolb & Gibb, 2008). Nevertheless, greater therapeutic gains are made with infants and toddlers than neurologically mature individuals (Bruder, 2010;Grafman, 2000;Zwaigenbaum et al., 2013), possibly due to reorganization of existing neuronal networks or the development of novel synaptic networks during rapid neurological growth in young neurological systems (Kolb & Gibb, 2008). ...
Purpose The purpose of this tutorial is to (a) provide an updated review of the literature pertaining to proposed early features of childhood apraxia of speech (CAS), (b) discuss the findings of recent treatment studies of infants and toddlers with suspected CAS (sCAS), and (c) present evidence-based strategies and tools that can be used for the identification of and intervention for infants and toddlers with sCAS or at high risk for the disorder. Method Since Davis and Velleman's (2000) seminal work on assessment and intervention in infants and toddlers with sCAS, limited research has guided clinicians in the complex task of identifying and treating early speech motor difficulties prior to a definitive diagnosis of CAS. Following the structure of Davis and Velleman, we explore the proposed early characteristics of CAS with reference to contemporary research. Next, we describe the limited treatment studies that have investigated intervention for infants and toddlers at risk of or suspected of having CAS. Finally, we present practical suggestions for integrating this knowledge into clinical practice. Conclusions Many of the originally proposed correlates of CAS in infants and toddlers now have research supporting their presence. However, questions remain about the developmental trajectory of the disorder. Although limited in number and restricted by lack of experimental control, emerging treatment studies can help guide clinicians in providing appropriate intervention to infants and toddlers with sCAS who need not wait for a definitive diagnosis to initiate intervention.
... With inadequate reading eye movements, these corrective saccades resulted in an increased number of fixations and regressions. 23 The efficacy of vision therapy in improving oculomotor skills in mTBI has been reported by Thiagarajan et al. where oculomotor training resulted in significant improvements in reading rate and vergenceaccommodation amplitude. ...
... 5,22 The potential of the brain to change its structural and functional response to the diversity of the environment is known as brain plasticity. 23 A network of billions of glia and neurons travel to their respective locations, establishing a flexible network. Repeated stimulation with increased synaptic strength causes biochemical, cellular, physiological, and structural changes. ...
Reading involves adequate coordination of the oculomotor system. As interlink consists of neuronal control, an insult to the brain might affect the signal processing and lead to oculomotor dysfunction that can affect reading performance. Appropriate training to enhance the oculomotor coordination is effective in such scenarios. The purpose of this case report is to highlight the role of neuro-optometric vision therapy as a management option in oculomotor-based reading difficulty.
... Among the deficits caused by physiological aging are changes in cognitive functions. Studies in the field of neuroscience have shown that through neuroplasticity it is possible to remodel and reorganize the brain's structure and function in the elderly (Demarin et al., 2014;Kolb & Gibb, 2015). The term neuroplasticity is multifaceted (Voss et al., 2017) and addresses a large number of possibilities that allow brain changes to be generated. ...
... Consequently, there is atrophy of brain lobes, with possible progressive shrinking of cells, and reduced synaptic density (Arcos-Burgos et al., 2019). These transformations can alter the volume of white matter, causing lapses in the functioning of neuronal transmission, especially in areas of the prefrontal cortex, associated with working memory and executive function (EF) (Kolb & Gibb, 2015). ...
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This study aimed to summarize investigations that examined the benefits of dance on the neuroplasticity of older healthy adults, report structural and functional changes in the brain, and identify the strategies used in training protocols. The integrative review was perfomed in PubMed, Web of Science and Scopus databases, including randomized clinical trials, quasi-experimental, cross-sectional and cohort studies published in English, between 2010-2020. Twelve articles ware selected. Dance practice was associated with an improvement in functional connectivity, cognitive performance, and incresead brain volumes. Our results main supports studies on the plasticity induced by dance training in healthy older people.
... A partir de leur soma, de forme triangulaire, naissent les dendrites recouvertes d'épines : les dendrites basales, qui naissent à la base du soma et les dendrites apicales, qui naissent à l'apex du soma. Adapté de Kolb and Gibb, 2015 ...
Les épines dendritiques sont de petites protrusions membranaires qui portent la partie postsynaptique des synapses excitatrices. Les épines sont des structures extrêmement dynamiques : elles subissent des changements de forme et de fonction qui dépendent d’une réorganisation dynamique du cytosquelette d’actine. En effet, la dynamique de l’actine régule la forme de l’épine ainsi que la force de transmission synaptique. L’actine influence cette activité synaptique à travers le contrôle du nombre et de la localisation des récepteurs AMPA (AMPARs), qui assurent la transmission excitatrice rapide. Parmi les protéines qui régulent la dynamique de l’actine, la cofiline, une protéine qui dépolymérise l’actine, favorise le renouvellement dynamique de l’actine. L’inactivation de la cofiline par sa phosphorylation par la LIMK augmente la stabilité de l’actine, ce qui conduit à des altérations de forme d’épine et à un défaut de recrutement des AMPARs pendant la plasticité synaptique. Des anomalies de la dynamique des épines et de leur fonction sont une caractéristique de la plupart des pathologies neuropsychiatriques.La maladie de Huntington (MH) est une pathologie neurodégénérative et génétique caractérisée par la dysfonction et la dégénérescence des neurones du striatum et du cortex adultes. Les symptômes apparaissent à l’âge adulte et incluent des manifestations motrices, cognitives et psychiatriques. La MH est causée par la mutation du gène qui code pour la protéine huntingtine (HTT). Jusqu’à présent, la plupart des études se sont concentrées sur le gain de nouvelles fonctions toxiques de la HTT mutée. Cependant, on considère désormais que les évènements conduisant à la manifestation clinique de la MH sont en partie dus à la modification des fonctions de la HTT normale. La compréhension des fonctions normales de cette protéine est donc cruciale pour élucider les mécanismes cellulaires à l’origine de la MH.Nous montrons que la perte de HTT pendant le développement altère la morphologie des épines dendritiques et l’activité des synapses chez le jeune animal. Plus précisément, la HTT est présente dans le compartiment postsynaptique, et sa déplétion de façon cellule-autonome augmente le nombre d’épines matures et réduit la transmission synaptique excitatrice dépendante des AMPARs. Les AMPARs sont en effet affectés par la perte de HTT, puisque cette dernière réduit leur expression postsynaptique et limite leur recyclage à la suite d’une stimulation synaptique. Le cytosquelette d’actine est par ailleurs plus stable dans les épines déplétées en HTT, et ceci est associé à une hyperactivité de la voie moléculaire RAC1-LIMK-Cofiline. Ces résultats apportent de nouvelles informations quant aux fonctions moléculaires de la HTT dans la régulation de la morphologie des épines et de la physiologie de la synapse, processus qui pourrait être altéré dans le contexte de la MH.
... Mason et al. 2006;Bliss-Moreau et al. 2011Kazama et al. 2012;Moadab et al. 2015) and the hippocampus (e.g. Banta Lavenex et al. 2006;Lavenex and Lavenex 2006), with critical periods for plasticity identified in infancy (Kolb 1989;O'Leary et al. 1994;Kolb and Gibb 2010). Although infancy appears to be the period in which the most significant neural plasticity can and does occur (Ismail et al. 2017;Kolb et al. 2017), there is growing recognition that the adult brain-once thought to be fairly static and incapable of large structural changes-also has a remarkable ability to compensate for damage, including both microstructural and macrostructural changes (Burke and Barnes 2006;Hübener and Bonhoeffer 2014;Power and Schlaggar 2017). ...
Accumulating evidence indicates that the adult brain is capable of significant structural change following damage—a capacity once thought to be largely limited to developing brains. To date, most existing research on adult plasticity has focused on how exteroceptive sensorimotor networks compensate for damage to preserve function. Interoceptive networks—those that represent and process sensory information about the body’s internal state—are now recognized to be critical for a wide range of physiological and psychological functions from basic energy regulation to maintaining a sense of self, but the extent to which these networks remain plastic in adulthood has not been established. In this report, we used detailed histological analyses to pinpoint precise changes to gray matter volume in the interoceptive-allostatic network in adult rhesus monkeys (Macaca mulatta) who received neurotoxic lesions of the anterior cingulate cortex (ACC) and neurologically intact control monkeys. Relative to controls, monkeys with ACC lesions had significant and selective unilateral expansion of the ventral anterior insula and significant relative bilateral expansion of the lateral nucleus of the amygdala. This work demonstrates the capacity for neuroplasticity in the interoceptive-allostatic network which, given that changes included expansion rather than atrophy, is likely to represent an adaptive response following damage.
... Neuroplasticity is governed not only by changes in afferent stimuli secondary to tissue damage but is also experiencedependent secondary to behavioral changes, new experiences, or training [80]. Experience-dependent neuroplasticity can be reparative, where new networks or connections are formed in an attempt to restore or maintain function or developmen- tal, where synaptic formation and pruning occur to learn or refine a skill [112,113]. In the context of movement, both principles underlie mechanisms for motor learning, the process for motor skill acquisition/improvement that result in relatively permanent changes in performance, which is the goal of rehabilitation. ...
Background Despite surgical reconstruction and extensive rehabilitation, persistent quadriceps inhibition, gait asymmetry, and functional impairment remain prevalent in patients after anterior cruciate ligament (ACL) injury. A combination of reports have suggested underlying central nervous system adaptations in those after injury govern long-term neuromuscular impairments. The classic assumption has been to attribute neurophysiologic deficits to components of injury, but other factors across the continuum of care (e.g. surgery, perioperative analgesia, and rehabilitative strategies) have been largely overlooked. Objective This review provides a multidisciplinary perspective to 1) provide a narrative review of studies reporting neuroplasticity following ACL injury in order to inform clinicians of the current state of literature and 2) provide a mechanistic framework of neurophysiologic deficits with potential clinical implications across all phases of injury and recovery (injury, surgery, and rehabilitation) Results Studies using a variety of neurophysiologic modalities have demonstrated peripheral and central nervous system adaptations in those with prior ACL injury. Longitudinal investigations suggest neurophysiologic changes at spinal-reflexive and corticospinal pathways follow a unique timecourse across injury, surgery, and rehabilitation. Conclusion Clinicians should consider the unique injury, surgery, anesthesia, and rehabilitation on central nervous system adaptations. Therapeutic strategies across the continuum of care may be beneficial to mitigate maladaptive neuroplasticity in those after ACL injury.
... Insect species living in cooperative societies have brains capable of changing with colony needs and in response to features of social life (Gronenberg et al., 1996;Jaumann et al., 2019;O'Donnell, 2007, 2008;O'Donnell et al., 2007;Rehan et al., 2015;Smith et al., 2010;Withers et al., 1993Withers et al., , 1995. This neuroplasticity, i.e. changes in neural structure and function over a lifetime (Kolb and Gibb, 2008), comes in two formsexperience-dependent and experience-expectant. Whether each form evolved prior to or in response to sociality is unknown. ...
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In social insects, changes in behavior are often accompanied by structural changes in the brain. This neuroplasticity may come with experience (experience-dependent) or age (experience-expectant). Yet, the evolutionary relationship between neuroplasticity and sociality is unclear, because we know little about neuroplasticity in the solitary relatives of social species. We used confocal microscopy to measure brain changes in response to age and experience in a solitary halictid bee ( Nomia melanderi ). First, we compared the volume of individual brain regions among newly-emerged females, laboratory females deprived of reproductive and foraging experience, and free-flying, nesting females. Experience, but not age, led to significant expansion of the mushroom bodies—higher-order processing centers associated with learning and memory. Next, we investigated how social experience influences neuroplasticity by comparing the brains of females kept in the laboratory either alone or paired with another female. Paired females had significantly larger olfactory regions of the mushroom bodies. Together, these experimental results indicate that experience-dependent neuroplasticity is common to both solitary and social taxa, whereas experience-expectant neuroplasticity may be an adaptation to life in a social colony. Further, neuroplasticity in response to social chemical signals may have facilitated the evolution of sociality.
Investigation of the role of music in early life and learning has been somewhat fragmented, with studies being undertaken within a range of fields with little apparent conversation across disciplinary boundaries, and with an emphasis on preschoolers’ and school-aged children’s learning and engagement. The Oxford Handbook of Early Childhood Learning and Development in Music brings together leading researchers in infant and early childhood cognition, music education, music therapy, neuroscience, cultural and developmental psychology, and music sociology to interrogate questions of how our capacity for music develops from birth, and its contributions to learning and development. Researchers in cultural psychology and sociology of musical childhoods investigate those factors that shape children’s musical learning and development and the places and spaces in which children encounter and engage with music. These issues are complemented with consideration of the policy environment at local, national, and global levels in relation to music early learning and development and the ways these shape young children’s music experiences and opportunities. The handbook also explores issues of music provision and developmental contributions for children with special education needs, children living in medical settings and participating in music therapy, and those living in sites of trauma and conflict. Consideration of these environments provides a context to examine music learning and development in family, community, and school settings including general and specialized school environments. Authors trace the trajectories of development within and across cultures and settings and identify those factors that facilitate or constrain children’s early music learning and development.
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A well-documented phenomenon among social insects is that brain changes occur prior to or at the onset of certain experiences, potentially serving to prime the brain for specific tasks. This insight comes almost exclusively from studies considering developmental maturation in females. As a result, it is unclear whether age-related brain plasticity is consistent across sexes, and to what extent developmental patterns differ. Using confocal microscopy and volumetric analyses, we investigated age-related brain changes coinciding with sexual maturation in the males of the facultatively eusocial sweat bee, Megalopta genalis, and the obligately eusocial bumble bee, Bombus impatiens. We compared volumetric measurements between newly eclosed and reproductively mature males kept isolated in the lab. We found expansion of the mushroom bodies—brain regions associated with learning and memory—with maturation, which were consistent across both species. This age-related plasticity may, therefore, play a functionally-relevant role in preparing male bees for mating, and suggests that developmentally-driven neural restructuring can occur in males, even in species where it is absent in females.
Objective: Neuroplasticity enables the brain to establish new crossmodal connections or reorganize old connections which are essential to perceiving a multisensorial world. The intent of this review is to identify and summarize the current developments in neuroplasticity and crossmodal connectivity, and deepen understanding of how crossmodal connectivity develops in the normal, healthy brain, highlighting novel perspectives about the principles that guide this connectivity. Methods: To the above end, a narrative review is carried out. The data documented in prior relevant studies in neuroscience, psychology and other related fields available in a wide range of prominent electronic databases are critically assessed, synthesized, interpreted with qualitative rather than quantitative elements, and linked together to form new propositions and hypotheses about neuroplasticity and crossmodal connectivity. Results: Three major themes are identified. First, it appears that neuroplasticity operates by following eight fundamental principles and crossmodal integration operates by following three principles. Second, two different forms of crossmodal connectivity, namely direct crossmodal connectivity and indirect crossmodal connectivity, are suggested to operate in both unisensory and multisensory perception. Third, three principles possibly guide the development of crossmodal connectivity into adulthood. These are labeled as the principle of innate crossmodality, the principle of evolution-driven 'neuromodular' reorganization and the principle of multimodal experience. These principles are combined to develop a three-factor interaction model of crossmodal connectivity. Conclusions: The hypothesized principles and the proposed model together advance understanding of neuroplasticity, the nature of crossmodal connectivity, and how such connectivity develops in the normal, healthy brain.
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Chronic restraint stress causes significant dendritic atrophy of CA3 pyramidal neurons that reverts to baseline within a week. Therefore, the authors assessed the functional consequences of this atrophy quickly (within hours) using the Y maze. Experiments 1-3 demonstrated that rats relied on extrinsic, spatial cues located outside of the Y maze to determine arm location and that rats with hippocampal damage (through kainic acid, colchicine, or trimethyltin) had spatial memory impairments. After the Y maze was validated as a hippocampally relevant spatial task, Experiment 4 showed that chronic restraint stress impaired spatial memory performance on the Y maze when rats were tested the day after the last stress session and that tianeptine prevented the stress-induced spatial memory impairment. These data are consistent with the previously demonstrated ability of tianeptine to prevent chronic stress-induced atrophy of the CA3 dendrites.
Many patients with brain damage are left with a range of neuropsychological deficits that impair normal cognitive process. It is generally recognised that these less obvious cognitive deficits (including memory, language, perception, attention, and executive disorders) militate against full recovery often to a greater extent than more traditional medical deficits (e.g. paralysis, sensory loss, etc.). Recognition of this has helped fuel the exponential growth in cognitive neuropsychology and neuroscience over the past thirty years. In turn, this theoretical approach has been used to guide and inform the development of cognitive therapies designed to remediate cognitive impairments and their functional consequences. Cognitive rehabilitation has over the last decade grown to become an established and influential therapeutic approach. There is now a considerable body of knowledge describing the principles and theoretical basis for analysing and directing treatments to selective cognitive deficits. Despite this, the clinical effectiveness and extent to which cognitive theory can inform therapeutic treatment has been questioned. It is timely, therefore, to evaluate and discuss the type and quality of evidence used in support of cognitive rehabilitation.
With an ever increasing population of aging people in the western world, it is more crucial than ever that we try to understand how and why cognitive competence breaks down with advancing age why do some people follow normal patterns of cognitive change, while others follow a path of progressive decline, with neurodegenerative diseases such as Alzheimer's. What can be done to prevent cognitive decline or - to avoid neurodegenerative diseases? The answers, if they come, will not emerge from research within one discipline, but from work being done across a range of scientific and medical specialities. This book delves into the subjects of cognitive aging, neuroscience, pharmacology, health, genetics, sensory biology, and epidemiology. This book is about new frontiers rather than past research and accomplishments. Recently cognitive aging research has taken several new directions, linking with, and benefiting from, rapid technological and theoretical advances in these neighbouring disciplines. This book provides unique interdisciplinary coverage of the topic. © Roger A. Dixon, Lars Bäckman, and Lars Göran-Nilsson 2004. All rights reserved.
My heartfelt thanks to Johannes Menzel, Senior Publishing Editor at Elsevier, for offering me the opportunity to be part of the production team of these four volumes of essays on the evolution of nervous systems. I was excited about being among the first to read the essays. We are all likely to be curious about ourselves, in particular, about how we acquired the complex brain that allows us our human abilities. Thus, a central question is how our brain evolved from the simple nervous systems of an ancient nonvertebrate ancestor, as the organization of our brain reflects not only adaptations for present-day functions, but also the history of a torturous evolutionary path. The essays help us understand that path. We are also likely to be curious about how the many different types of nervous systems came to be. As a researcher focused on studying nervous systems, I am impressed that there are over 4500 species of mammals, all with nervous systems that are different while more or less resembling each other. However, mammals make up just a small portion of the animals with nervous systems, and it is challenging to comprehend, let alone understand, all the diversity in central nervous system organization that must exist. How can we make sense of all this diversity? Fortunately, as in all biology, patterns emerge that reflect evolution. All animal life can be traced back to a common ancestor, and the great variety in nervous systems that exists is the result of imperfect copying of the genetic code from generation to generation as shaped by selection. With little or no lateral gene transfer across lines of descent, complex animal life represents a true hierarchy with a single beginning and multiple branching points. This phylogenetic structure means that nervous systems more or less resemble each other, with accumulated differences that reflect times of branching and rates of change. This relationship greatly simplifies the task of understanding the diversity that exists. The essays in the four volumes provide at least a good start toward that understanding.
Many patients with brain damage are left with a range of neuropsychological deficits that impair normal cognitive process. It is generally recognised that these less obvious cognitive deficits (including memory, language, perception, attention, and executive disorders) militate against full recovery often to a greater extent than more traditional medical deficits (e.g. paralysis, sensory loss, etc.). Recognition of this has helped fuel the exponential growth in cognitive neuropsychology and neuroscience over the past thirty years. In turn, this theoretical approach has been used to guide and inform the development of cognitive therapies designed to remediate cognitive impairments and their functional consequences. Cognitive rehabilitation has over the last decade grown to become an established and influential therapeutic approach. There is now a considerable body of knowledge describing the principles and theoretical basis for analysing and directing treatments to selective cognitive deficits. Despite this, the clinical effectiveness and extent to which cognitive theory can inform therapeutic treatment has been questioned. It is timely, therefore, to evaluate and discuss the type and quality of evidence used in support of cognitive rehabilitation.
Declarative memory declines with age, but there is profound variation in the severity of this decline. Healthy elderly adults with high or low memory scores and young adults viewed words under semantic or non-semantic encoding conditions while undergoing fMRI. Young adults had superior memory for the words, and elderly adults with high memory scores had better memory for the words than those with low memory scores. The elderly with high scores had left lateral and medial prefrontal activations for semantic encoding equal to the young, and greater right prefrontal activation than the young. The elderly with low scores had reduced activations in all three regions relative to the elderly with high memory scores. Thus, successful aging was characterized by preserved left prefrontal and enhanced right prefrontal activation that may have provided compensatory encoding resources.
In mammals comparable lesions of the cerebral cortex affecting motor status have far less permanent and severe effect when the injury is sustained in infancy than when it occurs in maturity.¹ This is apparent in all species in which adult motor performance is largely dominated by the cerebral cortex, as in man, monkey, dog and cat.² Thus, when the cortical areas 4 and 6 of Brodmann are removed from infant monkeys or chimpanzees, there is little immediate effect on motor performance and only moderate effects appear as such animals later develop.³ In contrast, adult animals exhibit severe paresis after similar procedures (figs. 1 and 2). The processes, anatomic or physiologic, which lie behind this striking age difference are unknown. Even the relationship of myelination to function is not certain, although much discussed. This paper deals with one obvious and immediate step in further analysis of the question,