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Brain plasticity refers to the brain's ability to change structure and function. Experience is a major stimulant of brain plasticity in animal species as diverse as insects and humans. It is now clear that experience produces multiple, dissociable changes in the brain including increases in dendritic length, increases (or decreases) in spine density, synapse formation, increased glial activity, and altered metabolic activity. These anatomical changes are correlated with behavioral differences between subjects with and without the changes. Experience-dependent changes in neurons are affected by various factors including aging, gonadal hormones, trophic factors, stress, and brain pathology. We discuss the important role that changes in dendritic arborization play in brain plasticity and behavior, and we consider these changes in the context of changing intrinsic circuitry of the cortex in processes such as learning.
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Copyright © 2003 American Psychological Society
1
CURRENT DIRECTIONS IN PSYCHOLOGICAL SCIENCE
Abstract
Although the brain was once
seen as a rather static organ, it is
now clear that the organization
of brain circuitry is constantly
changing as a function of expe-
rience. These changes are re-
ferred to as brain plasticity,
and they are associated with
functional changes that include
phenomena such as memory,
addiction, and recovery of
function. Recent research has
shown that brain plasticity and
behavior can be influenced by
a myriad of factors, including
both pre- and postnatal experi-
ence, drugs, hormones, matu-
ration, aging, diet, disease, and
stress. Understanding how
these factors influence brain
organization and function is
important not only for under-
standing both normal and ab-
normal behavior, but also for
designing treatments for be-
havioral and psychological dis-
orders ranging from addiction
to stroke.
Keywords
addiction; recovery; experi-
ence; brain plasticity
One of the most intriguing ques-
tions in behavioral neuroscience
concerns the manner in which the
nervous system can modify its or-
ganization and ultimately its func-
tion throughout an individual’s
lifetime, a property that is often re-
ferred to as
plasticity.
The capacity
to change is a fundamental charac-
teristic of nervous systems and can
be seen in even the simplest of or-
ganisms, such as the tiny worm
C.
elegans
, whose nervous system has
only 302 cells. When the nervous
system changes, there is often a
correlated change in behavior or
psychological function. This behav-
ioral change is known by names
such as learning, memory, addiction,
maturation, and recovery. Thus, for
example, when people learn new
motor skills, such as in playing a
musical instrument, there are plas-
tic changes in the structure of cells
in the nervous system that underlie
the motor skills. If the plastic
changes are somehow prevented
from occurring, the motor learning
does not occur. Although psychol-
ogists have assumed that the ner-
vous system is especially sensitive
to experience during develop-
ment, it is only recently that they
have begun to appreciate the po-
tential for plastic changes in the
adult brain. Understanding brain
plasticity is obviously of consider-
able interest both because it pro-
vides a window to understanding
the development of the brain and
behavior and because it allows in-
sight into the causes of normal and
abnormal behavior.
THE NATURE OF BRAIN
PLASTICITY
The underlying assumption of
studies of brain and behavioral plas-
ticity is that if behavior changes,
there must be some change in orga-
nization or properties of the neural
circuitry that produces the behav-
ior. Conversely, if neural networks
are changed by experience, there
must be some corresponding change
in the functions mediated by those
networks. For the investigator inter-
ested in understanding the factors
that can change brain circuits, and
ultimately behavior, a major chal-
lenge is to find and to quantify the
changes. In principle, plastic changes
in neuronal circuits are likely to re-
flect either modifications of exist-
ing circuits or the generation of
new circuits. But how can research-
ers measure changes in neural cir-
cuitry? Because neural networks
are composed of individual neu-
rons, each of which connects with a
subset of other neurons to form in-
terconnected networks, the logical
place to look for plastic changes is
at the junctions between neurons,
that is, at synapses. However, it is a
daunting task to determine if syn-
apses have been added or lost in a
particular region, given that the
human brain has something like
100 billion neurons and each neuron
makes on average several thousand
synapses. It is clearly impractical to
scan the brain looking for altered
synapses, so a small subset must be
identified and examined in detail.
But which synapses should be
studied? Given that neuroscientists
have a pretty good idea of what re-
gions of the brain are involved in
particular behaviors, they can nar-
row their search to the likely areas,
but are still left with an extraordi-
narily complex system to examine.
There is, however, a procedure that
makes the job easier.
In the late 1800s, Camillo Golgi
invented a technique for staining a
random subset of neurons (1–5%)
so that the cell bodies and the den-
dritic trees of individual cells can
be visualized (Fig. 1). The den-
drites of a cell function as the scaf-
folding for synapses, much as tree
branches provide a location for
leaves to grow and be exposed to
sunlight. The usefulness of Golgi’s
technique can be understood by
pursuing this arboreal metaphor.
There are a number of ways one
Brain Plasticity and Behavior
Bryan Kolb,
1
Robbin Gibb, and Terry E. Robinson
Canadian Centre for Behavioural Neuroscience, University of Lethbridge, Lethbridge,
Alberta, Canada (B.K., RG.), and Department of Psychology, University of Michigan,
Ann Arbor, Michigan (T.E.R.)
2 VOLUME 12, NUMBER 1, FEBRUARY 2003
Published by Blackwell Publishing Inc.
could estimate how many leaves are
on a tree without counting every leaf.
Thus, one could measure the total
length of the tree’s branches as well
as the density of the leaves on a
representative branch. Then, by sim-
ply multiplying branch length by
leaf density, one could estimate to-
tal leafage. A similar procedure is
used to estimate synapse number.
About 95% of a cell’s synapses are
on its dendrites (the neuron’s
branches). Furthermore, there is a
roughly linear relationship be-
tween the space available for syn-
apses (dendritic surface) and the
number of synapses, so researchers
can presume that increases or de-
creases in dendritic surface reflect
changes in synaptic organization.
FACTORS AFFECTING BRAIN
PLASTICITY
By using Golgi-staining proce-
dures, various investigators have
shown that housing animals in
complex versus simple environ-
ments produces widespread differ-
ences in the number of synapses in
specific brain regions. In general,
such experiments show that partic-
ular experiences embellish cir-
cuitry, whereas the absence of
those experiences fails to do so
(e.g., Greenough & Chang, 1989).
Until recently, the impact of these
neuropsychological experiments
was surprisingly limited, in part
because the environmental treat-
ments were perceived as extreme
and thus not characteristic of
events experienced by the normal
brain. It has become clear, how-
ever, not only that synaptic organi-
zation is changed by experience,
but also that the scope of factors
that can do this is much more ex-
tensive than anyone had antici-
pated. Factors that are now known
to affect neuronal structure and be-
havior include the following:
experience (both leading pre-
and post-natal)
psychoactive drugs (e.g., amphet-
amine, morphine)
gonadal hormones (e.g., estrogen,
testosterone)
anti-inflammatory agents (e.g.,
COX-2 inhibitors)
growth factors (e.g., nerve growth
factor)
dietary factors (e.g., vitamin and
mineral supplements)
genetic factors (e.g., strain differ-
ences, genetically modified mice)
disease (e.g., Parkinson’s disease,
schizophrenia, epilepsy, stroke)
stress
brain injury and leading disease
We discuss two examples to illus-
trate.
Early Experience
It is generally assumed that ex-
periences early in life have differ-
ent effects on behavior than similar
experiences later in life. The reason
for this difference is not under-
stood, however. To investigate this
question, we placed animals in
complex environments either as ju-
veniles, in adulthood, or in senes-
cence (Kolb, Gibb, & Gorny, 2003).
It was our expectation that there
would be quantitative differences in
the effects of experience on synaptic
organization, but to our surprise, we
also found
qualitative
differences.
Thus, like many investigators be-
fore us, we found that the length of
dendrites and the density of syn-
Fig. 1. Photograph of a neuron. In the view on the left, the dendritic field with the
extensive dendritic network is visible. On the right are higher-power views of den-
dritic branches showing the spines, where most synapses are located. If there is an
increase in dendritic length, spine density, or both, there are presumed to be more
synapses in the neuron.
Copyright © 2003 American Psychological Society
CURRENT DIRECTIONS IN PSYCHOLOGICAL SCIENCE 3
apses were increased in neurons in
the motor and sensory cortical re-
gions in adult and aged animals
housed in a complex environment
(relative to a standard lab cage). In
contrast, animals placed in the
same environment as juveniles
showed an increase in dendritic
length but a decrease in spine den-
sity. In other words, the same envi-
ronmental manipulation had quali-
tatively different effects on the
organization of neuronal circuitry
in juveniles than in adults.
To pursue this finding, we later
gave infant animals 45 min of daily
tactile stimulation with a little
paintbrush (15 min three times per
day) for the first 3 weeks of life.
Our behavioral studies showed
that this seemingly benign early
experience enhanced motor and
cognitive skills in adulthood. The
anatomical studies showed, in ad-
dition, that in these animals there
was a decrease in spine density but
no change in dendritic length in
cortical neurons—yet another pat-
tern of experience-dependent neu-
ronal change. (Parallel studies have
shown other changes, too, including
neurochemical changes, but these
are beyond the current discussion.)
Armed with these findings, we then
asked whether prenatal experience
might also change the structure of
the brain months later in adulthood.
Indeed, it does. For example, the off-
spring of a rat housed in a complex
environment during the term of her
pregnancy have increased synaptic
space on neurons in the cerebral cor-
tex in adulthood. Although we do
not know how prenatal experiences
alter the brain, it seems likely that
some chemical response by the
mother, be it hormonal or otherwise,
can cross the placental barrier and al-
ter the genetic signals in the develop-
ing brain.
Our studies showing that expe-
rience can uniquely affect the de-
veloping brain led us to wonder if
the injured infant brain might be
repaired by environmental treat-
ments. We were not surprised to
find that postinjury experience,
such as tactile stroking, could mod-
ify both brain plasticity and behav-
ior because we had come to believe
that such experiences were power-
ful modulators of brain develop-
ment (Kolb, Gibb, & Gorny, 2000).
What was surprising, however,
was that prenatal experience, such
as housing the pregnant mother in
a complex environment, could af-
fect how the brain responded to an
injury that it would not receive un-
til after birth. In other words, pre-
natal experience altered the brain’s
response to injury later in life. This
type of study has profound impli-
cations for preemptive treatments
of children at risk for a variety of
neurological disorders.
Psychoactive Drugs
Many people who take stimu-
lant drugs like nicotine, amphet-
amine, or cocaine do so for their
potent psychoactive effects. The
long-term behavioral consequences
of abusing such psychoactive
drugs are now well documented,
but much less is known about how
repeated exposure to these drugs
alters the nervous system. One ex-
perimental demonstration of a very
persistent form of drug experience-
dependent plasticity is known as
behavioral sensitization. For exam-
ple, if a rat is given a small dose of
amphetamine, it initially will show
a small increase in motor activity
(e.g., locomotion, rearing). When
the rat is given the same dose on
subsequent occasions, however,
the increase in motor activity in-
creases, or sensitizes, and the ani-
mal may remain sensitized for
weeks, months, or even years, even
if drug treatment is discontinued.
Changes in behavior that occur as
a consequence of past experience,
and can persist for months or years,
like memories, are thought to be due
to changes in patterns of synaptic or-
ganization. The parallels between
drug-induced sensitization and
memory led us to ask whether the
neurons of animals sensitized to
drugs of abuse exhibit long-lasting
changes similar to those associated
with memory (e.g., Robinson &
Kolb, 1999). A comparison of the ef-
fects of amphetamine and saline
treatments on the structure of neu-
rons showed that neurons in am-
phetamine-treated brains had greater
dendritic material, as well as more
densely organized spines. These
plastic changes were not found
throughout the brain, however, but
rather were localized to regions such
as the prefrontal cortex and nu-
cleus accumbens, both of which are
thought to play a role in the reward-
ing properties of these drugs. Later
studies have shown that these drug-
induced changes are found not only
when animals are given injections by
an experimenter, but also when ani-
mals are trained to self-administer
drugs, leading us to speculate that
similar changes in synaptic organi-
zation will be found in human drug
addicts.
Other Factors
All of the factors we listed earlier
have effects that are conceptually
similar to the two examples that
we just discussed. For instance,
brain injury disrupts the synaptic
organization of the brain, and
when there is functional improve-
ment after the injury, there is a cor-
related reorganization of neural
circuits (e.g., Kolb, 1995). But not
all factors act the same way across
the brain. For instance, estrogen
stimulates synapse formation in
some structures but reduces syn-
apse number in other structures
(e.g., Kolb, Forgie, Gibb, Gorny, &
Rowntree, 1998), a pattern of
change that can also be seen with
some psychoactive drugs, such as
morphine. In sum, it now appears
that virtually any manipulation
4 VOLUME 12, NUMBER 1, FEBRUARY 2003
Published by Blackwell Publishing Inc.
that produces an enduring change
in behavior leaves an anatomical
footprint in the brain.
CONCLUSIONS AND ISSUES
There are several conclusions to
draw from our studies. First, expe-
rience alters the brain, and it does
so in an age-related manner. Second,
both pre- and postnatal experience
have such effects, and these effects
are long-lasting and can influence
not only brain structure but also
adult behavior. Third, seemingly
similar experiences can alter neu-
ronal circuits in different ways, al-
though each of the alterations is
manifest in behavioral change.
Fourth, a variety of behavioral con-
ditions, ranging from addiction to
neurological and psychiatric disor-
ders, are correlated with localized
changes in neural circuits. Finally,
therapies that are intended to alter
behavior, such as treatment for ad-
diction, stroke, or schizophrenia,
are likely to be most effective if
they are able to further reorganize
relevant brain circuitry. Further-
more, studies of neuronal structure
provide a simple method of screen-
ing for treatments that are likely to
be effective in treating disorders
such as dementia. Indeed, our
studies show that the new genera-
tion of antiarthritic drugs (known
as COX-2 inhibitors), which act to re-
duce inflammation, can reverse age-
related synaptic loss and thus ought
to be considered as useful treatments
for age-related cognitive loss.
Although much is now known
about brain plasticity and behav-
ior, many theoretical issues re-
main. Knowing that a wide vari-
ety of experiences and agents can
alter synaptic organization and
behavior is important, but leads to
a new question: How does this
happen? This is not an easy ques-
tion to answer, and it is certain
that there is more than one an-
swer. We provide a single exam-
ple to illustrate.
Neurotrophic factors are a class
of chemicals that are known to af-
fect synaptic organization. An ex-
ample is fibroblast growth factor-2
(FGF-2). The production of FGF-2 is
increased by various experiences,
such as complex housing and tactile
stroking, as well as by drugs such as
amphetamine. Thus, it is possible
that experience stimulates the pro-
duction of FGF-2 and this, in turn,
increases synapse production. But
again, the question is how. One
hypothesis is that FGF-2 somehow
alters the way different genes are
expressed by specific neurons and
this, in turn, affects the way synapses
are generated or lost. In other words,
factors that alter behavior, including
experience, can do so by altering gene
expression, a result that renders the
traditional gene-versus-environment
discussions meaningless.
Other issues revolve around the
limits and permanence of plastic
changes. After all, people encounter
and learn new information daily. Is
there some limit to how much cells
can change? It seems unlikely that
cells could continue to enlarge and
add synapses indefinitely, but what
controls this? We saw in our studies
of experience-dependent changes in
infants, juveniles, and adults that ex-
perience both adds and prunes syn-
apses, but what are the rules govern-
ing when one or the other might
occur? This question leads to another,
which is whether plastic changes in
response to different experiences
might interact. For example, does ex-
posure to a drug like nicotine affect
how the brain changes in learning a
motor skill like playing the piano?
Consider, too, the issue of the perma-
nence of plastic changes. If a person
stops smoking, how long do the nico-
tine-induced plastic changes persist,
and do they affect later changes?
One additional issue surrounds
the role of plastic changes in disor-
dered behavior. Thus, although
most studies of plasticity imply
that remodeling neural circuitry is
a good thing, it is reasonable to
wonder if plastic changes might
also be the basis of pathological be-
havior. Less is known about this
possibility, but it does seem likely.
For example, drug addicts often
show cognitive deficits, and it
seems reasonable to propose that at
least some of these deficits could
arise from abnormal circuitry, es-
pecially in the frontal lobe.
In sum, the structure of the brain
is constantly changing in response
to an unexpectedly wide range of
experiential factors. Understanding
how the brain changes and the rules
governing these changes is impor-
tant not only for understanding
both normal and abnormal behav-
ior, but also for designing treat-
ments for behavioral and psycho-
logical disorders ranging from
addiction to stroke.
Recommended Reading
Kolb, B., & Whishaw, I.Q. (1998). Brain
plasticity and behavior.
Annual Re-
view of Psychology, 49
, 43–64.
Robinson, T.E., & Berridge, K.C. (in
press). Addiction.
Annual Review
of Psychology.
Shaw, C.A., & McEachern, J.C.
(2001).
Toward a theory of neuro-
plasticity.
New York: Taylor and
Francis.
Acknowledgments—
This research was
supported by a Natural Sciences and
Engineering Research Council grant to
B.K. and a National Institute on Drug
Abuse grant to T.E.R.
Note
1. Address correspondence to Bryan
Kolb, CCBN, University of Lethbridge,
Lethbridge, AB, Canada T1K 3M4.
References
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Copyright © 2003 American Psychological Society
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The Malicious Serpent: Snakes as a
Prototypical Stimulus for an Evolved
Module of Fear
Arne Öhman
1
and Susan Mineka
Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden (A.Ö.),
and Department of Psychology, Northwestern University, Evanston, Illinois (S.M.)
Abstract
As reptiles, snakes may
have signified deadly threats
in the environment of early
mammals. We review findings
suggesting that snakes remain
special stimuli for humans. In-
tense snake fear is prevalent in
both humans and other pri-
mates. Humans and monkeys
learn snake fear more easily
than fear of most other stimuli
through direct or vicarious
conditioning. Neither the elici-
tation nor the conditioning of
snake fear in humans requires
that snakes be consciously per-
ceived; rather, both processes
can occur with masked stimuli.
Humans tend to perceive illu-
sory correlations between
snakes and aversive stimuli,
and their attention is automati-
cally captured by snakes in
complex visual displays. To-
gether, these and other findings
delineate an evolved fear mod-
ule in the brain. This module is
selectively and automatically
activated by once-threatening
stimuli, is relatively encapsu-
lated from cognition, and de-
rives from specialized neural
circuitry.
Keywords
evolution; snake fear; fear
module
Snakes are commonly regarded
as slimy, slithering creatures worthy
of fear and disgust. If one were to be-
lieve the Book of Genesis, humans’
dislike for snakes resulted from a
divine intervention: To avenge the
snake’s luring of Eve to taste the fruit
of knowledge, God instituted eternal
enmity between their descendants.
Alternatively, the human dislike of
snakes and the common appear-
ances of reptiles as the embodiment
of evil in myths and art might reflect
an evolutionary heritage. Indeed,
Sagan (1977) speculated that human
fear of snakes and other reptiles
may be a distant effect of the condi-
tions under which early mammals
evolved. In the world they inhabited,
the animal kingdom was dominated
by awesome reptiles, the dinosaurs,
and so a prerequisite for early mam-
mals to deliver genes to future gen-
erations was to avoid getting caught
in the fangs of Tyrannosaurus rex
and its relatives. Thus, fear and re-
spect for reptiles is a likely core
mammalian heritage. From this
perspective, snakes and other rep-
tiles may continue to have a special
psychological significance even for
humans, and considerable evi-
dence suggests this is indeed true.
Furthermore, the pattern of find-
ings appears consistent with the
evolutionary premise.
THE PREVALENCE OF SNAKE
FEARS IN PRIMATES
Snakes are obviously fearsome
creatures to many humans. Agras,
Sylvester, and Oliveau (1969) inter-
viewed a sample of New England-
ers about fears, and found snakes
to be clearly the most prevalent ob-
ject of intense fear, reported by
38% of females and 12% of males.
Fear of snakes is also common
among other primates. According
to an exhaustive review of field
data (King, 1997), 11 genera of pri-
mates showed fear-related responses
(alarm calls, avoidance, mobbing) in
virtually all instances in which they
were observed confronting large
snakes. For studies of captive pri-
mates, King did not find consistent
evidence of snake fear. However,
in direct comparisons, rhesus (and
squirrel) monkeys reared in the
wild were far more likely than lab-
reared monkeys to show strong
phobiclike fear responses to snakes
(e.g., Mineka, Keir, & Price, 1980).
That this fear is adaptive in the
wild is further supported by inde-
pendent field reports of large
snakes attacking primates (M.
Cook & Mineka, 1991).
This high prevalence of snake
fear in humans as well as in our
... Following loss of peripheral input, the subcortical and cortical centers in the ascending auditory pathway adapt to the loss of afferent input, a compensatory process known as neural plasticity (Kolb and Whishaw, 1998). As such, the processing in subcortical and cortical centers is often described in terms of a gain with respect to the input-output function in the auditory system. ...
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... Structural changes can influence functional activity, while functional abnormalities can, in turn, result in alterations to the structure of corresponding brain regions. This reciprocal interaction is supported by the concepts of "functional plasticity" (brain function changes as compensatory mechanisms to structural damage), and "structural plasticity" (the brain's ability to reorganize its structure in response to functional demands) 61 . Notably, prolonged cord compression syndrome in DCM leads to both functional disruptions within the spinal cord and brain regions involved in sensory and motor processing, potentially inducing long-lasting structural modifications. ...
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... KANs effectively operate in a space of functions that are inherently more expressive and adaptable than those defined by fixed parametric forms. When the constituent functions ϕ q and ψ q,p are parameterized using flexible basis functions such as B-splines, Gaussian kernels, or Fourier series, the network gains the ability to approximate a wide variety of smooth, discontinuous, and high-frequency functions with relatively shallow architectures [13]. Theoretical investigations into the approximation properties of KANs reveal that they can achieve exponential convergence rates in certain function spaces, particularly Sobolev and Hölder spaces, depending on the smoothness of the target function and the spline degree. ...
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... Environmental signals sculpt brain development, resulting in changes in overall behavior 28 and physiology (Kolb & Whishaw, 1998;Meaney, 2001 was not certified by peer review) is the author/funder. All rights reserved. ...
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Day length, or seasonal photoperiod, shapes mood and affective behaviors but the neural mechanisms underlying these effects are still being defined. Serotonin neurons of the dorsal raphe nucleus (DRN) are critical regulators of affective behaviors and photoperiod modulates their excitability and ongoing activity. Here, we investigated the influence of seasonal photoperiod on the function and expression of small conductance calcium activated potassium (SK) channels which mediate the afterhyperpolarizing potential (AHP) in dorsal raphe serotonin neurons. Building on previous work demonstrating that photoperiod modulates serotonergic excitability and behavior, we hypothesized that day length influences SK channel activity, thereby contributing to differences in neuronal excitability observed between Long, Equinox, and Short photoperiod conditions. Using multi electrode array recording of DRN slices we found a significant dose dependent increase in spike rate to the application of the SK channel inhibitor apamin, indicating that SK channels indeed influence the spike rate of dorsal raphe serotonin neurons. In addition, DRN neurons in slices from Long photoperiod mice exhibited less pronounced responses to apamin relative to those from Short photoperiod mice, suggesting reduced function or expression of SK channels in Long photoperiod. Indeed, whole cell recordings demonstrated that SK channel mediated AHP currents were reduced in Long photoperiod mice. However, there were no significant differences in expression levels of the SK3 subunit (Kcnn3) in DRN serotonin neurons across photoperiod conditions as determined by single molecule fluorescence in situ hybridization. Overall, these findings indicate that photoperiod modulates SK channel function in DRN serotonin neurons likely at a post transcriptional level. This study advances our understanding of how seasonal cues influence intrinsic neuronal properties and provides a mechanistic link between photoperiod, serotonergic excitability, and mood-related behaviors. The identification of SK channels as modulators of photoperiodic effects may offer novel therapeutic targets for mood disorders associated with dysregulated serotonin signaling.
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The quotative system is a highly dynamic domain characterised by competing traditional variants (say, think) and newcomers (be all, be like) (Buchstaller 2013). Trend and apparent time studies have focused on be like, describing its expansion across the English-speaking world and reporting incrementation amongst the younger age-brackets (D' Arcy & Tagliamonte 2003; Gardner et al. 2021). "Information on speakers' loyalty to be like across their lifespan is conflicting", however (Buchstaller 2015: 460). We report on a dynamic panel corpus to assess malleability in the quotative system across the adult lifespan. Our findings suggest that the grammar underlying be like remains largely stable across the lifespan. And while most socio-demographic factors do not significantly influence speakers' quotative choices, we seem to witness the development of socially niched retrenchment in the middle age brackets, turning one of the most vibrant changes in the English language into a gender-differentiated and age-graded pattern.
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In this study, it was aimed to reveal the effect of regular life kinetic exercises on the concepts of motivation and imagery in sports in puberty period individuals. In the study in which “pre-test-post-test control group design” was used, 44 students (experiment = 22, control = 22) who were continuing their education in a state secondary school and selected by appropriate sampling method participated. The “Personal Information Form”, “Motivation Scale in Sport” and “Imagery Inventory in Sport” were used as data collection tools. The collected data were analysed using repeated measures analysis of variance. When the results were analysed, it was determined that there were statistically significant differences in the pre-test and post-test mean scores of motivation and imagery in sport. As a result, it can be stated that the life kinetic exercise protocol applied for 8 weeks in sedentary individuals positively predicted motivation and imagery parameters in sports. This result indicates that the related psychological phenomena, which are as important as sport performance in sports, can be positively affected by cognitive and motoric exercise combinations.
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This interdisciplinary work offers a comprehensive analysis of paradoxes and paradoxical thinking, exploring their manifestations in philosophy, societal dynamics, personality, and neuroscience. Demonstrating various methods for the augmentation of creativity and improved performance, this book uniquely integrates theoretical perspective with case studies and practical applications. As such it elucidates the theory and mechanisms of transforming the apparently impossible into the possible, illustrated by cases of social innovators successfully addressing insurmountable challenges. Aimed at graduate and postgraduate social science students and scholars, with over 500 bibliographical references, the text remains accessible to a broader audience due to its engaging language. Emphasizing the significance of paradoxes and paradoxical thinking in both professional and everyday contexts, it provides a nuanced exploration of paradoxical phenomena, making it a valuable resource for academic and general readers alike.
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Background and Purpose Heroin and cocaine users tailor their dosage, frequency and administration route to maximise the drugs' effects or prevent withdrawal symptoms. Counterintuitively, preclinical self‐administration and choice experiments employ, almost invariably and regardless of the pharmacokinetic properties of the drug under examination, fixed unit‐doses and timeouts (after unit‐doses) largely resulting in uniform drug‐taking patterns. This uniformity contrasts with the large variability observed in humans, which serves as critical indicator of addiction severity and treatment success. Here, by combining behavioural and pharmacokinetics assessments, we revealed that drug self‐administration procedures without timeouts may overcome this limitation. Experimental Approach We analysed heroin‐ and cocaine‐taking patterns and seeking and estimated drug‐brain levels in the presence or absence of timeout under different training conditions. Key Results Removing timeouts had a profound effect on heroin‐taking patterns and seeking, promoting the emergence of burst‐like intake, yielding higher brain peak concentrations of heroin. In contrast, the removal of timeout had marginal impact on cocaine‐taking patterns and seeking. Conclusion and Implications The removal of timeout during self‐administration revealed distinct cocaine and heroin patterns, with the latter closely resembling human heroin use patterns.
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Glucocorticoids (GCs) are secreted by the adrenal gland and mediate numerous adaptations to acute stress. Because many of these adaptations are catabolic in nature, prolonged GC exposure can ultimately be deleterious. This review presents evidence that damage to neurons of the hippocampus is among the deleterious effects of chronic GC-exposure. The hippocampus is a principal neural target tissue for the steroids, with high concentrations of GC receptors. The rate of hippocampal neuron loss appears sensitive to cumulative GC exposure over the lifespan: decreased concentrations retard senescent neuron loss while chronic exposure accelerates the process. The extent of this loss after acute insults such as hypoxia-ischemia or excitotoxic seizures is simularly sensitive to GC concentrations. GCs appear to induce a general metabolic vulnerability in hippocampal neurons, impairing their capacity to survive varied insults. This GC action occurs directly, rather than secondarily to peripheral GC actions; moreover, the pattern is GC-specific, as non-GC steroids do not potentiate the damage of hippocampal insults. Finally, an important component of the phenomenon may involve the inhibition of hippocampal neuronal glucose uptake by GCs, leaving neurons more vulnerable to any coincident metabolic challenges. These studies suggest that GC administration in the aftermath of hypoxia-ischemia or seizure may worsen hippocampal damage, while attentuation of endogenous GC secretion at that time might well prove protective of the structure.
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Focuses on age-associated changes in neural systems that are thought to be involved in learning and memory. Work with young animals has revealed that synaptic connections between neurons can be added or structurally altered by some types of experience. Although this type of neural plasticity persists into old age, it is apparently vulnerable to pathological factors typically associated with senescence, such as impaired blood flow or increased levels of stress hormones. Also examined is preliminary work suggesting that physical exercise may have positive effects on the aging brain. (French abstract) (PsycINFO Database Record (c) 2012 APA, all rights reserved)