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Principles of neuroplasticity and behavior
Bryan Kolb and Robbin Gibb
Introduction
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 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 brains 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 & 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 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.
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.
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Reference
Task learning
Gonadal hormones and stress
hormones
Psychoactive drugs (e.g.,
stimulants, THC)
Neurotrophic factors (e.g., NGF,
bFGF)
Natural rewards (e.g., social
interaction, sex)
Ageing
Stress
Anti-inflammatories (e.g., COX-2
inhibitors)
Diet (e.g., choline)
Electrical stimulation: kindling
LTP
Direct cortical stimulation
enduring changes, ranging from general sensorymotor 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 environments rather than simple laboratory cages, within
30 days there is about a 5% increase in brain weight
and cortical thickness, an increase in cortical acetylcholine 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
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NAcc show no response to the experience, but neither 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 experience with amphetamine, cocaine, or nicotine. An
obvious question was whether prior experience
with complex housing would interfere with drugdependent changes. It does. Animals given complex
housing experience prior to repeated doses of nicotine show a much attenuated response to the drug.
Another example of interactions in experiencedependent 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 dendritic 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 normal recovery from cortical injury in the second week
of life (Gibb & Kolb, unpublished).
Finally, we note that prenatal exposure to experiences described above interact with later postnatal
brain injury to produce differential changes in neuronal networks and correlated functional recovery. For
instance, rats given prenatal experience via their
mothers exposure to tactile stimulation or complex
housing show an attenuated effect of the later experience to perinatal brain injury and in some instances
show almost complete recovery that is correlated
with enhanced dendritic changes (Gibb et al., submitted). In contrast, rats exposed to stress or fluoxetine 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).
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Reference
Complex housing
Olfactory stimulation
Psychoactive drugs (e.g.,
stimulants)
Neurotrophic factors (e.g.,
nerve growth factor)
Anti-inflammatories (e.g.,
COX-2 inhibitors)
Electrical stimulation
Inosine
Antibodies to No-Go
Reference
provide human patients with some type of equivalent 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 amphetamine have given uneven results, likely because of
differences in lesion size. Laboratory studies suggest
that whereas rats with small lesions show a significant benefit of amphetamine, those with large
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Postscript
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 literature 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 cognitive rehabilitation.
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