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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.
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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
... Second, different regions of the brain are responsible for tasks and the two hemispheres function differently [81]. Third, the concept of brain plasticity suggests that the brain has the ability to change itself with respect to structure and function [18,46]. If we view one hemisphere as the human and the other hemisphere as the machine, we immediately obtain the brain metaphor of human-machine symbiosis in Fig. 4. The common SMV space ties together the human and the machine, serving a similar function of the corpus callosum in the brain. ...
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... In der bereits erwähnten Studie zum Verlauf großer Mediainfarkte und Blutungen spielte das Alter auch keine relevante Rolle und diese Patientengruppe war überwiegend älter als 60 Jahre. Tierexperimentell berichtet Kolb (1995) über vorhandene Lernfähigkeit von Ratten bis ins hohe Alter. Allerdings war diese nicht durch dieselbe Neuroplastizität vermittelt wie bei jungen Ratten: Letztere zeigten dendritisches sprouting, Erstere nicht. ...
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Zusammenfassung. Rehabilitation wird neben der Diagnostik zunehmend zu einem wesentlichen Standbein neuropsychologischer Tätigkeit. Versuche, den Inhalt und Prozess neuropsychologischer Rehabilitation theoretisch zu beschreiben, sind selten. In diesem Papier wird eine Interaktionstheorie zwischen neuropsychologischer Therapeutin bzw. neuropsychologischem Therapeut und Patient_in entwickelt. Im Zentrum dieses Vorschlags stehen die Thesen, dass neuropsychologische Therapie (aber auch Diagnostik) a) eine kognitive Umgebung konstruiert, in der Patient_innen die Erfahrung machen können, welche Funktionen durch die erlittene Läsion verändert wurden, b) darauf aufbauend eine geschützte kognitive Umgebung simuliert, die in der Komplexität den vorhandenen Fähigkeiten der Patient_innen gerade noch entspricht, c) eine Hierarchie von therapeutischen Cues anwendet, um den Patient_innen die geforderte Leistung des nächsten Schwierigkeitsgrades zu ermöglichen, d) diese Cues im wachsenden Maße ausschleicht, um den Patient_innen die Handlung selbstständigkeit zu ermöglichen. Ziel der Therapie ist damit ein dialogischer Prozess, der von zwei Polen ausgeht: dem Wunsch beider Parteien (Patient_in und Therapeut_in), Wiederherstellung der Leistungsfähigkeit zu erreichen, und der realistischen Wahrnehmung, auf welcher Stufe kognitiver Komplexität mit wie viel Anstrengung und therapeutischer Unterstützung maximale Selbstständigkeit möglich sein könnte. Zwischen diesen beiden Polen vermittelt die Prognose der Schädigung und diese muss durch das aktuelle Wissen um die Leistungsfähigkeit und Grenzen der bestmöglichen neuropsychologischen Therapie, also ihrer Evidenzbasierung, abgesichert sein. Die Prognose stellt sich gemäß den vulnerablen Phasen der Erholung (akute, subakute, chronische Phase) unterschiedlich und wird gleichzeitig durch die Interaktion zwischen Therapeut_in und Patient_in beeinflusst. Sie kann damit nicht allgemein gestellt werden, sondern nur entwickelt. Die Verpflichtung zur bestmöglichen Therapie impliziert, dass technische Neuerungen der Neurowissenschaften bekannt sein und potenziell angewandt werden müssen. Die Sichtweise der neuropsychologischen Therapie als Interaktion und Simulation einer geschützten kognitiven Umgebung stellt damit nicht nur den Gedanken der therapeutischen Kooperation in den Mittelpunkt, sie eröffnet gleichzeitig die Möglichkeit einer Wiederannäherung von klinischer Neuropsychologie und neurowissenschaftlicher Forschung.
... Positively, what can support our hypothesis are the research with fMRI revealing that Tai Chi Chuan promotes the plasticity of brain function. Brain plasticity refers to the ability to change brain structure and function under the influence of the environment (30). More evidence (31,32) confirmed that Tai Chi Chuan had a stronger ability to remodel brain function than general aerobic exercise, which was mainly reflected in the enhancement of FC between the left middle frontal gyrus and left parietal lobe. ...
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Numerous evidence has shown that patients with chronic fatigue syndrome (CFS) have changes in resting brain functional connectivity, but there is no study on the brain network effect of Tai Chi Chuan intervention in CFS. To explore the influence of Tai Chi Chuan exercise on the causal relationship between brain functional networks in patients with CFS, 21 patients with CFS and 19 healthy controls were recruited for resting-state functional magnetic resonance imaging (rs-fMRI) scanning and 36-item Short-Form Health Survey (SF-36) scale assessment before and after 1month-long training in Tai Chi Chuan. We extracted the resting brain networks using the independent component analysis (ICA) method, analyzed the changes of FC in these networks, conducted Granger causality analysis (GCA) on it, and analyzed the correlation between the difference causality value and the SF-36 scale. Compared to the healthy control group, the SF-36 scale scores of patients with CFS were lower at baseline. Meanwhile, the causal relationship between sensorimotor network (SMN) and default mode network (DMN) was weakened. The above abnormalities could be improved by Tai Chi Chuan training for 1 month. In addition, the correlation analyses showed that the causal relationship between SMN and DMN was positively correlated with the scores of Role Physical (RP) and Bodily Pain (BP) in CFS patients, and the change of causal relationship between SMN and DMN before and after training was positively correlated with the change of BP score. The findings suggest that Tai Chi Chuan is helpful to improve the quality of life for patients with CFS. The change of Granger causality between SMN and DMN may be a readout parameter of CFS. Tai Chi Chuan may promote the functional plasticity of brain networks in patients with CFS by regulating the information transmission between them.
... By adjusting the frequency of individual neural firings by adapting the connectivity between constituents, neurons can effectively shift their frequency timings to align their phases and collaboratively produce higher and more stable levels of influence in a neural network. In the human brain, the active adaptation of coupling strength between neurons is accomplished through synaptic and structural plasticity mechanisms [152]. ...
Article
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The human brain is a complex network whose ensemble time evolution is directed by the cumulative interactions of its cellular components, such as neurons and glia cells. Coupled through chemical neurotransmission and receptor activation, these individuals interact with one another to varying degrees by triggering a variety of cellular activity from internal biological reconfigurations to external interactions with other network agents. Consequently, such local dynamic connections mediating the magnitude and direction of influence cells have on one another are highly nonlinear and facilitate, respectively, nonlinear and potentially chaotic multicellular higher-order collaborations. Thus, as a statistical physical system, the nonlinear culmination of local interactions produces complex global emergent network behaviors, enabling the highly dynamical, adaptive, and efficient response of a macroscopic brain network. Microstate reconfigurations are typically facilitated through synaptic and structural plasticity mechanisms that alter the degree of coupling (magnitude of influence) neurons have upon each other, dictating the type of coordinated macrostate emergence in populations of neural cells. These can emerge in the form of local regions of synchronized clusters about a center frequency composed of individual neural cell collaborations as a fundamental form of collective organization. A single mode of synchronization is insufficient for the computational needs of the brain. Thus, as neural components influence one another (cellular components, multiple clusters of synchronous populations, brain nuclei, and even brain regions), different patterns of neural behavior interact with one another to produce an emergent spatiotemporal spectral bandwidth of neural activity corresponding to the dynamical state of the brain network. Furthermore, hierarchical and self-similar structures support these network properties to operate effectively and efficiently. Neuroscience has come a long way since its inception; however, a comprehensive and intuitive understanding of how the brain works is still amiss. It is becoming evident that any singular perspective upon the grandiose biophysical complexity within the brain is inadequate. It is the purpose of this paper to provide an outlook through a multitude of perspectives, including the fundamental biological mechanisms and how these operate within the physical constraints of nature. Upon assessing the state of prior research efforts, in this paper, we identify the path future research effort should pursue to inspire progress in neuroscience.
... Buna göre, amigdaladaki hücresel ve sinaptik değişimler nötr durumlara da duygusal tepkiler verilmesine sebep olurlar (Boyle, 2013;Fanselow ve LeDoux, 1999;Maren, 2003). Plastisite terimi temel olarak beyin yapısının deneyimler doğrultusunda değişikliğe uğramasını temsil etmektedir; bellek sistemleri ve öğrenmeyle doğrudan ilişkilidir (Kleim ve Jones, 2008;Kolb ve Whishaw, 1998;Livingston, 1966;). Bu kategoriye ek olarak, amigdalanın diğer bellek sistemleri üzerindeki modülatör etkisi üzerine olan çalışmalar da literatürde önemli bir yer edinmiştir (Ferry, Roozendaal ve McGaugh, 1999;Packard ve Teather, 1998;Roozendaal, Brunson, Holloway, McGaugh ve Baram, 2002). ...
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Full-text available
z Bu derleme çalışmasının amacı, belirli psikopatolojilerin incelenmesinde ve tedavisinde daha etkili seçeneklerin geliştirilmesine katkı sağlayabileceği düşünülen çoklu bellek sistemleri teorisini klinik psikoloji alan yazınına tanıtmaktır. Öncelikle psikopatolojinin tanımına ve disiplinler arası çalışmaların günümüzdeki önemine yer vererek başlayan çalışma, devamında çoklu bellek sistemlerini ve bu sistemlerin gelişimsel süreçte takip ettiği basamakları açıklamaktadır. Son olarak stres temelli bozukluklar, nörogelişimsel bozukluklar ve ergenlik dönemi psikopatolojilerinin açıklanmasında çoklu bellek sistemleri bakış açısının rolüne bu alanda yapılan çalışmaları derleyerek açıklık getirmektedir. Buna göre çoklu bellek sistemleri bakış açısı, her birinin ayrı ve geniş çaplı etiyolojik çalışmaları bulunan psikopatolojilerin ortak yönü olarak bellek ve öğrenme süreçleri ile bu süreçlerin altında yatan nörobiyolojiye vurgu yapmaktadır. Bu ortak yönlerin anlaşılması, özellikle eş tanılı rahatsızlıkların (örneğin; dikkat eksikliği ve hiperaktivite bozukluğu ile Turet sendromu) etiyolojisinin daha iyi açıklanmasına katkıda bulunabilir. Bununla birlikte; günümüz teknolojisi yardımıyla çoklu bellek sistemlerinden sorumlu ilgili beyin bölgelerinin uyarılması yoluyla izlenen davranışsal müdahale çalışmalarının, psikopatolojilere özgü semptomların azaltılmasında etkili olduğu gözlemlenmiştir. Çoklu bellek sistemlerini esas alarak geliştirilen ve farklı tanı gruplarını hedef alan benzer müdahalelerin etkililiğinin ileriki araştırmalar ile test edilmesi gerekmektedir. Abstract The aim of this review article is to introduce multiple memory systems theory to the clinical psychology literature, as this theory might contribute to the understanding of some of the psychopathologies and the development of more effective treatment options. The article starts with a definition of psychopathology and the importance of multidisciplinary research at present. It follows with the explanation of multiple memory systems and the developmental trajectory of these systems. Finally, the role of multiple memory systems perspective for stress related disorders, neurodevelopmental disorders and adolescence psychopathologies are explained with a review of the literature. According to that, multiple memory systems perspective highlights memory and learning processes and the underlying neurobiology as common points of different diagnoses, each of which has a separate and wide etiological research. Considering these common points might be important, especially for having a better insight for the etiology of comorbid disorders such as comorbid diagnosis of attention and hyperactivity disorder and Tourette's syndrome. In addition, the studies indicate that the behavioral interventions targeting the brain areas responsible for multiple memory systems have ameliorating effects on symptomatology, with the help of today's technological facilities. Further studies are needed for testing the effectiveness of similar interventions, which are based on multiple memory systems perspective, for targeting different diagnostic groups. Kuramsal Derleme
... If the neural circuits underlying these cognitivebehavioural abilities essential for general intelligence and lifetime adaptability are under-or abnormally-developed before adulthood, then it is likely that these changes will persist into early and middle adulthood and be more vulnerable to accelerated neurodegeneration in late adulthood. Brain development occurs in stages and is marked by periods of massive plasticity (i.e., major neuronal and synaptic rearrangement), particularly the perinatal and periadolescent transitions, the latter of which is characterized by significant gray matter reductions and white matter increases that correspond to cognitive-behavioural maturation [77][78][79]. Neuroimaging studies of connectivity in the brain suggest several dynamic brain networks governing executive functions, intelligence, and social-emotional behaviour emerge early in brain development, increase their functional interactions during adolescence, and variations in patterns of connectivity can predict healthy and pathological trajectories of development into adulthood [22,[80][81][82]. Changes in these cortical networks are thought to be influenced by early environmental experiences, including childhood abuse [83], urban upbringing [84], and screen time [33], and may have serious lifetime impacts on general cognitive ability, social-emotional behaviour, psychopathology, and substance use and abuse. ...
Article
Converging evidence from biopsychosocial research in humans and animals demonstrates that chronic sensory stimulation (via excessive screen exposure) affects brain development increasing the risk of cognitive, emotional, and behavioural disorders in adolescents and young adults. Emerging evidence suggests that some of these effects are similar to those seen in adults with symptoms of mild cognitive impairment (MCI) in the early stages of dementia, including impaired concentration, orientation, acquisition of recent memories (anterograde amnesia), recall of past memories (retrograde amnesia), social functioning, and self-care. Excessive screen time is known to alter gray matter and white volumes in the brain, increase the risk of mental disorders, and impair acquisition of memories and learning which are known risk factors for dementia. Chronic sensory overstimulation (i.e., excessive screen time) during brain development increases the risk of accelerated neurodegeneration in adulthood (i.e., amnesia, early onset dementia). This relationship is affected by several mediating/moderating factors (e.g., IQ decline, learning impairments and mental illness). We hypothesize that excessive screen exposure during critical periods of development in Generation Z will lead to mild cognitive impairments in early to middle adulthood resulting in substantially increased rates of early onset dementia in later adulthood. We predict that from 2060 to 2100, the rates of Alzheimer’s disease and related dementias (ADRD) will increase significantly, far above the Centres for Disease Control (CDC) projected estimates of a two-fold increase, to upwards of a four-to-six-fold increase. The CDC estimates are based entirely on factors related to the age, sex, race and ethnicity of individuals born before 1950 who did not have access to mobile digital technology during critical periods of brain development. Compared to previous generations, the average 17–19-year-old spends approximately 6 hours a day on mobile digital devices (MDD) (smartphones, tablets, and laptop computers) whereas individuals born before 1950 at the same age spent zero. Our estimates include the documented effects of excessive screen time on individuals born after 1980, Millennials and Generation Z, who will be the majority of individuals ≥65 years old. An estimated 4-to-6-fold increase in rates of ADRD post-2060 will result in widespread societal and economic distress and the complete collapse of already overburdened healthcare systems in developed countries. Preventative measures must be set in place immediately including investments and interventions in public education, social policy, laws, and healthcare.
Article
Electroencephalography was used to investigate the effects of extrastimulation and preterm birth on the development of visual motion perception during early infancy. Infants receiving extra motor stimulation in the form of baby swimming, a traditionally raised control group, and preterm born infants were presented with an optic flow pattern simulating forward and reversed self‐motion and unstructured random visual motion before and after they achieved self‐produced locomotion. Extrastimulated infants started crawling earlier and displayed significantly shorter N2 latencies in response to visual motion than their full‐term and preterm peers. Preterm infants could not differentiate between visual motion conditions, nor did they significantly decrease their latencies with age and locomotor experience. Differences in induced activities were also observed with desynchronized theta‐band activity in all infants, but with more mature synchronized alpha–beta band activity only in extrastimulated infants after they had become mobile. Compared with the other infants, preterm infants showed more widespread desynchronized oscillatory activities at lower frequencies at the age of 1 year (corrected for prematurity). The overall advanced performance of extrastimulated infants was attributed to their enriched motor stimulation. The poorer responses in the preterm infants could be related to impairment of the dorsal visual stream that is specialized in the processing of visual motion.
Article
Objective: Hemianopia following occipital stroke is believed to be mainly due to local damage at or near the lesion site. Yet, MRI studies suggest functional connectivity network (FCN) reorganization also in distant brain regions. Because it is unclear if reorganization is adaptive or maladaptive, compensating for, or aggravating vision loss, we characterized FCNs electrophysiologically to explore local and global brain plasticity and correlated FCN reorganization with visual performance. Methods: Resting-state EEG was recorded in chronic, unilateral stroke patients and healthy age-matched controls (n=24 each). The correlation of oscillating EEG activity was calculated with the imaginary part of coherence between pairs of interested regions, and FCN graph theory metrics (degree, strength, clustering coefficient) were correlated with stimulus detection and reaction time. Results: Stroke brains showed altered FCNs in the alpha- and beta-band in numerous occipital, temporal and frontal brain structures. On a global level, FCN had a less efficient network organization while on the local level node networks reorganized especially in the intact hemisphere. Here, the occipital network was 58% more rigid (with a more "regular" network structure) while the temporal network was 32% more efficient (showing greater "small-worldness"), both of which correlated with worse or better visual processing, respectively. Conclusions: Occipital stroke is associated with both local and global FCN reorganization, but this can be both, adaptive and maladaptive. We propose that the more "regular" FCN structure in the intact visual cortex indicates maladaptive plasticity where less processing efficacy with reduced signal/noise ratio may cause perceptual deficits in the intact visual field. In contrast, reorganization in intact temporal brain regions is presumably adaptive, possibly supporting enhanced peripheral movement perception.
Article
Zebrafish (Danio rerio) constitute a useful model for studying memory function and impairment in vertebrates and are now widely used in translational research. On the one hand, the adoption of simple, fast and reliable tests such as novel object recognition (NOR) has increased our knowledge considerable about memory mechanisms in animals. On the other hand, in many model organisms, exposure to environmental enrichment, especially during the early stages of development, affects various cognitive functions. Evidence for the effects of environmental enrichment on zebrafish has been accumulating rapidly, but most of this evidence has been collected in adult subjects. We compared larvae raised in either an enriched or barren environments and measured their memory performance at 14-days post-fertilization. Initially, subjects were allowed to familiarize with two identical novel objects (i.e., pattern of 2D-geometrical figures). After a time interval, larvae faced a two-choice task presenting the same objects paired with a new one. As a measure of recognition memory, we exploit the tendency of individuals to explore a novel object over a familiar one. Our results indicate that larvae from the barren environment spent more time exploring familiar stimuli than novel ones, showing the innate presence of recognition memory capacity in zebrafish larvae. Conversely, subjects bred in a visually enriched environment explore both familiar and novel stimuli almost equally. The increase of exploratory behaviour and, consequently, the reduction of avoidance to the novel object may explain the performance shown by larvae exposed to an enrichment environment compared to the larvae bred in a barren environment. Taken together, these results confirm that early-stage zebrafish possess complex visual discrimination capacities and that rearing subjects in a structurally complex environment might hinder memory performance by reducing their neophobic response.
Book
This book is the story of the marriage of a new techl}ology, computers, with an old problem, the study of neuroanatomical structures using the light microscope. It is aimed toward you, the neuroanatomist, who until now have used computers primarily for word processing but now wish to use them also to collect and analyze your laboratory data. Mter reading the book, you will be better equipped to use a computer system for data collection and analysis, to employ a programmer who might develop a system for you, or to evaluate the systems available in the marketplace. To start toward this goal, a glossary first presents commonly used terms in computer assisted neuroanatomy. This, on its own, will aid you as it merges the jargon of the two different fields. Then, Chapter 1 presents a historical review to describe the manual tasks involved in presenting and measuring anatomic structures. This review lays a base line of the tasks that were done before computers and the amount of skill and time needed to perform the tasks. In Chapters 2 and 3, you will find basic information about laboratory computers and programs to the depth required for you to use the machines easily and talk with some fluency to computer engineers, programmers, and salesmen. Chapters 4, 5, and 6 present the use of computers to reconstruct anatomic structures, i.e., to enter them into a computer memory, where they are later displayed and analyzed."
Chapter
In the late 1960s, Pat Bateson, Gabriel Horn and I began to work together on the cell biology of learning and memory, using imprinting in the young chick as a model. Other papers in this volume describe the elegant way in which the imprinting work has been continued by the Cambridge group. Here, I will review the results of the use of an alternative form of early learning in the young chick, based on a one trial passive avoidance task. The point is that, for the biochemist there are certain disadvantages to studying the sequelae of imprinting as a model for memory. The process of training by exposure to the stimulus is a relatively long one, and this makes it harder to distinguish the cellular events associated with putative memory storage processes from those which are the concomitants of the experience of training. Birds also show a degree of variability in their behaviour during training and the strength of their later preference which can be exploited experimentally but which also adds to the complexity of the analysis.
Chapter
Olfaction is only partly developed at birth in most altricial mammals (Altman 1969; Alberts 1982; Bayer 1983; Mair and Gesteland 1982; Mair et al. 1982; Schleidt and Hold 1982; Leon et al. 1984; Coopersmith and Leon this Vol; U. Schmidt this Vol). Since some parts seem to be more mature than others (Greer et al. 1982; Schwob et al. this Vol), the question arose as to whether the system as a whole is influenced by postnatal sensory and environmental experiences (cf. Schmidt, Meisami, Lü et al., Panhuber, all this Vol).
Article
The randomness of the impregnation of layer IV cortical neurons by the Golgi-Cox method (Van der Loos, 1956) has been assessed directly in Barrel C-1 of the mouse SmI. All Golgi-Cox impregnated neurons and unimpregnated neurons which were revealed with Nissl counterstain were counted and measured in ten cerebral hemispheres cut tangential to the pia overlying the barrel field. The percentage of Golgi stained neurons varied considerably in different preparations from 0.73% to 2.26% with an average of 1.29%. The size distributions of both the Golgi impregnated and Nissl stained cells are similar but the difference of the means is statistically significant. However, if the means are eqated there is no statistical difference in the two populations. When the Golgi precipitate is removed and the cells re-measured following Nissl staining there is a systematic reduction of the perikaryal cross-sectional area which is compatible with the differences in the means observed for the two populations as a whole. Finally, the frequency with which Golgi impregnated neurons are found in the barrel sides and hollows parallels the frequency with which Nissl stained neurons are observed in these two locations. We conclude that this variant of the Golgi method impregnates barrel neurons randomly. The value of this information for quantitative studies of cerebral cortex is discussed as is the potential of the system for elucidating some of the mechanisms responsible for Golgi impregnation.
Article
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.
Article
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)