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Chapter 6
Plastic Mind
We now leave general descriptions
of the evolution of hominid minds, psychology, and culture to turn to a more
detailed account of how those minds develop, the next theme we need in assembling
a description of the biology of our minds. The first part of this book has
outlined the increasing sophistication and complexity of animal and human minds
over evolutionary time, focusing mainly on the adult forms that mate and pass
their genes on to future generations. These minds and brains start out as a
mere blueprint, or template, provided by their genetic history, and then their
adult forms arise only through a complicated sequence of developmental steps.
To change the final product, the building blocks and/or the steps in their
construction have to be changed.
It is remarkable how labile, or
plastic, the construction of brains and minds can be. It varies because the
intimate details depend on the actual environment provided by other cells in
the developing embryo, on interactions between embryo and mother, and finally
on interactions of the brains and bodies of growing children with their physical
and social environment. Each of us has a unique brain whose formation is directed
by our early surroundings, language, and culture. The structures described
below form in a stereotyped and fairly constant way during embryonic development,
but after birth they continue to grow and can be molded and shaped by their
interaction with the outside world. This ensemble of evolutionary and individual
developmental history forms the adult "society of mind" that is the
subject of Part III of this book.
This chapter offers some evolutionary
arguments for why brain development has become more malleable in more complicated
animals, and it also describes the amazing plasticity that we can observe in
developing as well as adult brains. This plasticity underlies the effects that
both social experience and sexual differentiation have on brain processes,
and it is required for the changes in nerve connections that support memory
and learning. Our ability to remember facts and procedures---perhaps the most
striking example of our brain plasticity---is considered in this chapter. This
type of cognitive neuroscience is emphasized later, in Part III, but there
are two reasons for discussing it briefly here. First, similar changes in nerve
cell synapses seem to occur during nerve development and during the storage
of some kinds of memories. Second, the human "selves" whose construction
we consider in Chapter 7 are built from memories.
An Outline of Brain Development
Development consists of an intricate
sequence of cell divisions and migrations that create local environments whose
different chemistries turn different sets of genes on or off. Early development
is dominated by axial information systems (dorsal-ventral, head-tail) that
span the whole embryo and cause localized gene actions in different parts of
the growing embryo. Events at this stage show considerable developmental flexibility
and thus are a target for adaptive changes during evolution. Midway through
development, an intricate interconnectivity occurs between elements that will
later come to represent separate modules such as organ primordia (of brain,
heart, lung, liver, and so on). This developmental path restricts the flexibility
of the system, because changes in one module can alter many others. By late
development, however, more developmental flexibility is seen again because
the body has been highly modularized. At this point, adaptive changes in a
liver, for example, don't have to cause changes in nervous tissue. Similarly,
a genetic change that improves the effectiveness of a brain module doesn't
have to affect the kidney.
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DESIGN NOTE: LONG IMPORTANT POINT
The enormity of the problem we
face us when we try to understand the development of our brain can be illustrated
with some simple numbers. Our brains contain at least 1010 neurons with an
average of 104 nerve connections or synapses to each, yet the human genome
contains less than 105--6 genes. Thus there is no way that the position of
each nerve cell, much less each of the many connections made by that cell,
could be uniquely specified by a single gene. The problem is compounded by
the need for instructions to form all of the other organ systems of our bodies.
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We share with all vertebrates an
embryo that in its early stages is a flat plate made up of inner, middle, and
outer layers: endoderm, mesoderm, and ectoderm. Figure 6-1(a--c) shows cross
sections of an early embryo that indicate the way these layers fold to form
the neural tube from which the central nervous system develops. Figure 6-1(d)
shows a view of the neural tube from above, cut horizontally so that you can
see its interior. You can imagine this neural tube as a sausage-shaped balloon
filled with water (cerebrospinal fluid, or CSF). Three swellings at the front
end of the balloon form forebrain, midbrain, and hindbrain (you might find
it useful to refer to Figure 3-2, which offers a side view of these structures).
The forebrain further subdivides into a central portion (diencephalon) and
two vesicles (telencephalon) that sprout from it to form eventually the two
cerebral hemispheres that constitute our cerebral cortex. (Throughout this
bulging and folding process, the central CSF-containing channels are maintained
and become the ventricular system of the adult brain.) Two smaller vesicles
that sprout from the diencephalon become the optic nerve and retina. The diencephalon
finally differentiates into the thalamus and hypothalamus. The thalamus is
the gateway for information going to and from the cerebral cortex. The telencephalon
folds onto itself to form the hippocampus and olfactory cortex on its internal
and bottom surfaces. These structures are two cell layers thick. Then, only
in mammals, the top external part of the telencephalon forms the "new
cortex," or neocortex, which has six layers of nerve cells. When people
speak of the cerebral cortex, they usually mean the neocortex, even though "cortex" properly
refers to all of the structures derived from the telencephalon. Figure 6-2
provides simple summary drawings of the developing human brain, from the stage
of the neural tube shown in Figure 6-1 to the formation of the neocortex.
Figure 6-1
Formation of the neural tube, neural
crest, and brain vesicles. (a) The three basic cell types of the early embryo.
The endoderm generates many of our internal organs, the mesoderm generates
our bones and muscles, and the nervous system and skin come entirely from ectoderm.
A part of the ectoderm gives rise to the nervous system by forming a flat sheet
of cells called the neural plate. (b, c) A groove forms in this plate, and
the walls of the groove join to form the neural tube. The whole central nervous
system (CNS), consisting of spinal cord and brain, develops from this tube.
As this happens, some neural ectoderm pinches off just to the sides of the
neural tube. This is the neural crest that gives rise to the peripheral nervous
system (PNS) described in Chapter 3. (d) A view of the neural tube from above,
showing forebrain, midbrain, and hindbrain. Adapted from Figures 7.8 and 7.9
in Bear et al. Neuroscience : Exploring the Brain.
Figure 6-2
Changes in the structure of the
developing human brain. The first three drawings, which indicate the swellings
of the neural tube during the formation of forebrain, midbrain, and hindbrain,
are shown enlarged with respect to the later stages. These later stages show
the cerebral hemispheres overgrowing the midbrain and hindbrain, as well as
partly obscuring the cerebellum.
These brain structures, along with
those described in Chapter 3, provide us with a basic hard-wired ensemble of
automatic, reflexive, and instinctive mechanisms shaped by genetic trial and
error over many generations. If we put our hand on a hot stove, we need not
think about escaping as withdrawal reflexes take over, jerking it out of harm's
way. We share with other vertebrates hardwiring for fighting, fleeing, sex,
aggression, sleeping, and eating. Such hardwiring is centered in the primitive
mammalian brain, the limbic system, and in such other structures as the brainstem,
thalamus, and hypothalamus. The inferior temporal cortex of 5-week-old monkeys
contains neurons that respond to faces and complex geometrical patterns. Our
short-term and longer-term behaviors can be under instinctive control. We act
out daily, monthly, and annual cycles as we sleep and wake, produce fertile
eggs once a month, and undergo seasonal changes in mood and affect.
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DESIGN NOTE: IMPORTANT POINT
We are born with brains wired to
attend longer to stimuli that look like human faces than to other stimuli,
and our own faces register appropriate emotional responses.
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There is a problem, however, in
relying only on hardwired, or inflexible, behavioral routines that have been
crafted over millions of years of evolution. Just as they evolved slowly, they
can change only over many generations, as genes and developmental mechanisms
are altered, and numerous features of the environment change much faster than
that. The solution that evolved as brains became more complicated during evolution
was to make their formation more plastic---patterned by the actual surroundings
in which they must function. This permits human adaptation to an environment
to occur on the time scale of a single life span, rather than the many generations
that would be required for genetic selection within the population's gene pool.
Origins of Plasticity
Having a nervous system whose design
is completely predetermined by a fixed set of genes and developmental sequences
has one major drawback. If the environment changes suddenly, the animal may
be left with inflexible behaviors appropriate to the environment that shaped
its evolution but quite dysfunctional under the new conditions. A solution,
or adaptation, to this problem would be to have genes specify not one fixed
nervous system, but rather a starting array of options that can be tested for
their appropriateness as developing nerve connections and pathways are used
in the real world. Organisms
with the ability to select among developmental options should have an advantage
over those that cannot easily adapt to changing circumstances. Organisms that
have more plasticity should more effectively move toward a desirable adult
form---and so reproduce better. Their technique for achieving more plasticity
should then be passed on. A Darwin Machine mechanism of the sort described
in Chapter 2---preferential duplication of forms that work best---could act
on a developmental, rather than a generational, time scale to select and amplify
growing nerve pathways that work, at the expense of those that do not work
as well.
These options appear to have been
taken during the course of evolution. Pathways and competencies that do not
prove to be relevant during development do not mature. In
the case of feral human infants, raised by animals in the wild, normal language
and bipedal locomotion do not develop. The
close matching of their behavior with that of their surrogate animal parents
shows how little distinctively human behavior is obligatory in the absence
of a normal human cultural environment. In the right selective environment,
however, the brains of these children could have become the brains of airplane
pilots. Similarly, songbirds have a genetically programmed template that specifies
a range of sounds that can be learned, but the song actually performed is usually
learned from other birds. The rule seems to be "use it or never develop
it," a variant on "use it or lose it."
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DESIGN NOTE: IMPORTANT POINT
In more complicated animals, interaction
between the environment and neural growth leads to a flexible, constructive
kind of learning that minimizes the need for detailed prespecification of structures.
Selection dictates which of the many possible pathways are chosen and become
permanent.
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As birds learn to sing, and as
human babies learn to walk and produce language, there is room for variation
and change, but after this learning period, the design laid down becomes relatively
permanent. Thereafter, further learning is much more difficult. Once we have
learned to walk or ride a bicycle, we usually don't forget how to do it. But
learning to ride a bicycle after adolescence is much more difficult than when
we are under 10 years old. Similarly, a young human infant is a polyglot, able
to utter the sounds of any human language. But much of this potential range
is lost as soon as the language actually learned fixes the design of the infant's
language "pathways."
During brain growth there is a
constant sorting and juggling of nerve cells and connections. Those that make
a match with their environment thrive, and the others wither. Imagine what
it would be like to move in a visual world that consisted mainly of vertical
lines and contours---to be unable to see the horizon. Experiments on cats and
monkeys that we will soon describe suggest that this might happen to us if
we were shown only vertical stimuli for a year or so after our birth. Cells
that process vertical stimuli would grow to prevail over cells that deal with
horizontal lines, because our visual brains wire themselves to be most responsive
to the stimuli actually encountered early in life. There are critical periods
during which not only our visual brains but also many other areas, including
our social brains, are wired to conform to and accommodate the external environment.
If that early environment is degraded, so is the development of our mental
capacities.
A Hierarchy of Developmental Circuits
from Innate to Learned
We would expect innate circuits
that shape basic survival behaviors, such as approach/avoidance, to influence
circuits that can be modified by experience. Clusters of nerve cells, present
deep in our brainstem and common to all mammals, distribute neurotransmitters
such as serotonin, acetylcholine, dopamine, and norepinephrine to large areas
of our cortex and influence both the growth of the brain during development
and its behavior, as well as plasticity, in the adult. These
older innate circuits are responsive to what is happening to more modern sectors
of the brain and can signal the "goodness" or "badness" of
different situations. They are crucial components of the chemistry underlying
motivation. They react by influencing how the rest of the brain reacts, and
how it is shaped, so that it can become wired in the way that most effectively
supports survival. For example, it is most relevant to grow a brain that is
predisposed to register associations between illness and taste (rather than
between illness and place, sound, or temperature) and then, through learning,
determine which foods with which tastes actually lead to poisoning or illness.
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DESIGN NOTE: IMPORTANT POINT
A human child cannot be genetically
equipped with knowledge of who will be nurturing and who dangerous, but it
can be "told" by its genes that facial characteristics are important
indicators of this distinction.
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What we are describing is a hierarchy
of primary (genetic) and secondary (developmental) problem-solving devices.
The primary genetic mechanism acts on a generational time scale, and the secondary
process comes into play during postnatal development. This is the distinction
made by references to ultimate and proximal causes of human form and behavior.
The secondary, or proximal, process involves the growth and reinforcement of
neuronal pathways and connections that work best, as well as the atrophy of
those that are not found useful. This reinforcement comes not only from our
learning to move about in the immediate physical world but also from cultural
and social influences that guide our behavior and development.
Human genes and environments interact
on at least four levels in the construction of brains and selves: (1) Genes
instruct, and are instructed by, the complex internal environment of the fertilized
egg and by subsequent interactions between groups of dividing cells and tissues.
(2) They can be regulated by hormonal and other interactions between the developing
fetus and the maternal chemistry of the uterus. (3) Gene expression after birth
in infant humans, as in other animals, is patterned by the development of sensing
and acting routines appropriate to the species' typical physical environment.
(4) Individual social interactions among infant, caretaker, and peers then
pattern the learning of more complicated behaviors. Thus the influence of genes
is expressed through a long, tortuous, and indirect pathway.
The Wiring of Developing Brains
We now need to consider what is
known about brain developmental processes, and the ways in which they are shaped
by environmental changes. As we have noted, the brain originates as a swelling
at the head end of the spinal cord. Then a series of bulges and folds give
rise to the eyes and the lobes of the cortex, as nerve cell bodies migrate
to their final positions. Axons then grow out to make interconnections between
appropriate groups of nerve cells. A variety of mechanisms guide the growth
of axons as they find their targets in the brain. One mechanism is derivative
of the chemotaxis described in Chapter 2. A nerve cell body, or rather the
growing tip (called a growth cone) of its axon, can be attracted to move toward
a target that is releasing a particular growth factor to "call" the
growth cone (Figure 6-3). Physical cues, such as those that promote grow along
grooves or alongside other nerve cells, are also used. Some cells serve as
guideposts for the turnings or migrations of others. Ongoing neural activity---the
firing of nerve signals---is crucial in both the growing cells and their potential
targets.
Figure 6-3
The growth cone. If we look in
the microscope at the growing tip of an axon, we observe what appears to be
very intelligent purpose, just as in bacteria exhibiting chemotaxis. Delicate
little finger-like projections wave about and literally reach out to touch
and taste other cells in the growth path of the axons. The growth cone is repelled
by some such cells and attracted by others.
When a final target is encountered,
as, for instance, when a motor nerve axon finds the muscle that it will control,
the searching "fingers" retract, and both nerve and muscle respond
by making the pre- and postsynaptic structures that are required for a synapse.
A growing axon may make many temporary connections with other cells, acting
as though it is testing them for appropriateness, before moving on to its final
position. An important factor appears to be the functional appropriateness
of the tentative connections being made and remade. Are they useful in correlating
the input and output of the whole animal? Are they appropriate for the environment
in which the organism is functioning?
Pathways to the Cerebral Cortex
To consider what is happening in
more detail, we need a simple description of how sensory cells in the eye,
ear, or skin ultimately get their information to the cortex. Virtually all
of them connect to cells that pass through the thalamus, which has separate
nuclei, or groups of nerve cells, devoted to different kinds of input. The
lateral geniculate nucleus carries visual input to the visual cortex, the medial
geniculate nucleus carries sound information to the temporal cortex, the ventral
posterior lateral nucleus carries somatosensory information from the body to
the parietal cortex, and so on (Figure 6-4). The flow of information is bidirectional,
for the cortex also sends information back to the thalamus. There is strong
evidence that axon pathfinding between major structures such as the eye and
the thalamus, and the thalamus and the cortex, is under the control of genes. This
pathfinding also appears to require constant nerve activity.
Figure 6-4
Pathways from peripheral sense
organs enter lower brain areas and then pass through different nuclei of the
thalamus on their way to areas of the neocortex that are specialized for different
sensory modalities.
The cortex develops in two directions,
radially and tangentially. In the radial direction are six layers of nerve
cell bodies; layer 1 is on the top, and layer 6 on the bottom. Information
coming into the cortex goes primarily to layer 4, the "in box" of
the cortex. Cells of layers 5 and 6 send information back out to subcortical
brain regions (functioning as the "out box" of the cortex), and cells
in layers 1, 2, and 3 connect different cortical regions to each other, sort
of like an interoffice network for sending memoranda back and forth. As we
move across different regions of the cortex tangentially, these six layers
might be found to be supporting vision, hearing, commanding movements, and
so on. Their detailed structure varies in accordance with their different roles.
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DESIGN NOTE: LONG IMPORTANT POINT
It is currently thought that the
early cortex is not regionally specified and that the specialized areas form
as axons from the thalamus grow to them, bringing different kinds of stimulation
from the external world. It is almost as though various sensory surfaces---with
their specialized receptor cells sensing light, sound, pressure, and so on---impose
themselves onto the brainstem, then onto the thalamus, and finally onto the
cortex itself.
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Functional Plasticity in the Formation
of Cortical Areas
During the formation of these thalamus-to-cortex
pathways, dramatic plasticity at the cortical level can be observed, and specialized
cortical regions expand, contract, or take on functions other than their normal
ones if unusual circumstances are encountered. A number of experiments of the
sort shown in Figure 6-5 demonstrate that areas of cortex can switch from one
sensory mode to another. If one sensory modality is blocked at birth, areas
of cortex that normally serve it can be invaded by other sensory modes. Thus,
in cats deprived of visual input, the parts of the parietal cortex that are
usually predominantly visual are taken over by auditory and somatosensory input,
and these animals show greater sound and tactile discrimination than normal
animals. Another striking observation
is that in some congenitally blind humans, the visual cortex is activated by
reading Braille. This shows that input from the hand that normally goes primarily
to the somatosensory cortex can also be directed to visual areas in the occipital
lobe. One model is that at birth
the human cortex has synesthesia, mixing of the senses, and that the senses
become clearly separate only after about 4 months. Before this, in human babies,
electrical responses to spoken language are recorded not just over the auditory
regions of the temporal cortex but over the visual cortex as well. In the small
number of human adults who have synesthesia, such as those who see colors when
they hear sounds, the normal separation of the senses apparently has not occurred.
Figure 6-5
Switching cortical function from
one sensory mode to another. (a) Most of the input from the eye to the brain
goes through the lateral geniculate nucleus of the thalamus to the visual cortex
located at the back of the brain, but early in cortical development, a few
connections are also made to other parts of the thalamus (dashed line); these
connections normally are eliminated later in development. Similarly, sensations
at the body surface are sent mainly to the ventral posterior lateral nucleus
of the thalamus and then to somatosensory cortex in the parietal lobe located
in front of the occipital lobe, but again, some connections are made to other
parts of the thalamus and are later eliminated. (b) The experiment, begun early
in development, involves placing lesions in the lateral geniculate nucleus
and the visual cortex, as well as blocking input from the body surface to the
thalamus (as shown by the X's). Now input from the eye has lost its normal
targets but still has the few connections made to other areas of the thalamus
(dashed line, top). Also, the ventral posterior lateral (VPL) nucleus of the
thalamus and the somatosensory cortex are without their normal input. What
is observed is that the visual connections to the VPL nucleus (shown as the
dashed line in part a) can multiply and become a permanent visual input (solid
line) directed via the VPL nucleus to somatosensory cortex. This
somatosensory cortex takes on the function of visual cortex. In the same sort
of experiment, visual information can also be rerouted to the auditory cortex,
which then converts from representing the pitch and frequency of sound to representing
the locations of objects in the external world.
Other types of experiments further
demonstrate cortical plasticity. In the newborn rodent cortex, visual areas
can be transplanted to somatosensory areas take on somatosensory function,
and the reverse transfer also works. Auditory and visual cortex transplanted
onto each other also change their function. However, the transplants never
function in exactly the same way as the normal structures, which suggests that
they may have already been patterned by some thalamic input. Most of these
examples involve primary sensory areas, but a striking plasticity in higher
cortical functions is observed when, in newborn monkeys, the portion of the
temporal cortex responsible for visual object recognition (see Chapter 8) is
removed from both left and right cortexes. This function moves a considerable
distance to the part of the parietal lobe that normally deals with the movement
and orientation of objects in space.
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DESIGN NOTE: IMPORTANT POINT
Transplant experiments have demonstrated
cortical plasticity by showing that a cortical area that normally serves one
sensory modality can be transplanted and take on the functions of another.
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Plasticity in Forming the Visual
Cortex
Studies on the development of the
visual system, particularly the wiring of the cells in the occipital cortex
at the back of the brain, have provided several fascinating examples of how
labile the wiring-up process is and how susceptible it is to being changed
by distortions in the environment. Similar phenomena are found in all parts
of the brain, but the visual system has proved so accessible to experimentation
that many basic and pioneering studies have used it.
The primary visual cortex in the
occipital lobe of one hemisphere receives input from both eyes. If we move
an electrode along the surface of this cortex in adult cats or monkeys, we
find alternating rows of cells that respond mainly to one eye or to the other.
Studies on kittens and monkeys have shown that cells of the primary visual
cortex are driven by both eyes at birth, but one eye tends to dominate. During
the first 6 weeks of life, as the young animals learn to move about and use
their visual world to guide body movement, much clearer domains of cortex are
formed that respond mainly to one or the other eye. However, if visual information
from one eye is blocked during a critical period after birth (4--6 weeks in
the cat), either by putting an opaque contact lens in the eye or by temporarily
sewing the eyelids shut, the normal adult pattern is changed. Input from the
eye that remains open now expands to occupy a larger area of cortical surface,
while the area occupied by input from the closed eye contracts.
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DESIGN NOTE: IMPORTANT POINT
There seems to be an active competition
between the two eyes for cortical targets. Diminished input from one eye tells
the cortex that the active eye is more important and deserves more connections.
In other words: Use it or lose it!
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The playing out of this competition
requires that the cortical targets themselves also be actively communicating.
If their nerve signals are silenced by chemical inhibitors, inputs from the
closed eye expand. There appears
to be a push-pull mechanism of synaptic plasticity: When target cells are working
(are giving postsynaptic responses), the active eye has the advantage just
described, but without postsynaptic activity, the inactive inputs have an advantage. One
possible explanation is that activity from the active eye causes its target
cells in the cortex to release molecules (neurotrophins) that stimulate proliferation
of the active inputs. There
appear to be many ways in which the number and strength of synaptic connections
between cells can be altered. Figure 6-6 outlines some of these ways in a very
simplified form.
Figure 6-6
Ways in which altering nerve pathways
from different sources, such as suppressing input to the visual cortex from
the left but not the right eye, might influence the competition of the two
eyes for targets in the visual cortex. (a) The normal balance of input from
left and right eyes, via the lateral geniculate nucleus. (The example is simplified
to show only a few synaptic connections between cells. In reality, the axon
from a cell in the lateral geniculate nucleus might branch to make synapses
with hundreds to thousands of target cells in the cortex.) After suppression
of input from the left eye, increased activity might improve the effectiveness
of existing connections (b), disuse might lead to atrophy of the unused pathway
(c), and axons of the more active pathway might sprout branches that form new
synapses (d).
The story becomes even more interesting
as more subtle properties of visual cortical cells are examined. Most of these
cells are sensitive to the orientation of a visual stimulus, and cells that
respond to all directions of the compass are found at birth. If, however, a
young cat is exposed to an environment that contains mainly vertical bars during
the critical period when connections are formed, then cells sensitive to vertical
bars predominate in the adult visual cortex. As
is the case with the ocular dominance areas, a crude, genetically specified
pattern present at birth can be profoundly altered by the visual experience
actually encountered during the postnatal growth and development of the visual
system.
Experience Guides the Formation
of Successful Connections
Two processes appear to be central
in wiring up our brains: the pruning away of initial, exuberant overgrowth
of axons into their target areas, and elaboration of the complexity of the
connections that remain. The
first process has been likened to a Darwinian competition, including replication
of pathways, testing of their appropriateness, and enhanced survival of those
copies that work best. This selective process also probably works to test the
results of the invention, or construction, of the complex circuits used to
solve the problems specific to different kinds of information processing (visual,
auditory, somatosensory, and motor) throughout an extended period of brain
maturation. An example of a selection process---one that might guide both the
formation of new connections and the elimination of unnecessary ones---might
be the effectiveness of getting food from hand to mouth, which requires elaborate
circuits for hand-eye coordination. We are born with hardwiring set to do it
in a primitive and clumsy way. The pathways then grow and are refined through
testing. Another example is offered by development of the visual system. We
are born with cortical cells that detect stimuli of all orientations, but the
ability of human adults and many terrestrial animals to detect vertically or
horizontally oriented contours is superior to their ability to perceive oblique
angles. The prevalence of vertical and horizontal orientations in natural indoor
and outdoor settings apparently leads to increasing stimulation and growth
of visual cortical cells that specialize in those orientations. A further example
of how nerve cell wiring is influenced by functional testing is outlined in
the experiment shown in Figure 6-7.
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DESIGN NOTE: IMPORTANT POINT
What a brain is apparently doing
during the wiring up of its nerve cells is testing the functional appropriateness
of connections that are present or are being formed. Do those connections work
in guiding behavior in the real world?
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Figure 6-7
The sorting out of appropriate
nerve connections. An example of the determination of nerve connections by
functional testing comes from experiments in which a bundle of sensory nerves
running to the hand of a young monkey is severed. (a) Before the nerve to the
hand is cut, nerves in the fingers ultimately report, via the thalamus, to
adjacent parts of the somatosensory cortex: finger 1 goes to area 1 of thalamus
and then to area 1 of the brain, and so on. (We made these numbers up, just
to make our point. They don't refer to existing anatomical designations, used
by professional neuroanatomists, in thalamus or cortex.) If the bundle of nerves
to the hand is cut (dashed line), its distal end (the end farther from the
attachment) degenerates, but then its axons can be regenerated from the ends
of the nerves above the cut that are still connected to their cell bodies.
(b) These axons grow back to connect to the hand in a disordered fashion. Now
the axons reporting from finger 1 to the thalamus might be those that used
to report from finger 4, and so on, as shown by the crossed connections on
the right. Adjacent areas of the cortex should no longer represent adjacent
fingers. Quite to the contrary, however, the representation of this reinnervated
hand in the primary somatosensory cortex develops in a orderly fashion. The
developing brain is able to sort things out and create order, despite the fact
that its sensory inputs were temporarily scrambled. This suggests that the
pattern of sensory stimulation from the fingers is the most crucial cue for
establishing neighbor relationships in the part of the somatosensory cortex
that represents the hand, where adjacent areas of the cortex represent adjacent
fingers. The nerves from adjacent
fingers will be active together more frequently than the nerves from the first
and fifth fingers. Cells that fire together are then more likely to wire together!
Synapses that use the main excitatory transmitter of the brain, glutamic acid,
appear to play a central role in these examples of plasticity.
It is not clear how much of the
circuitry for higher mental functions is determined beforehand by genetic instructions,
and how much is discovered by each growing brain as it bootstraps its way to
maturity, growing through a series of stages of increasing complexity, each
of which makes use of the solutions to problems devised in earlier stages.
From what we now know about the molecular details of how nerve cells work,
we can see how such factors as the speed of nerve signals and the density of
connections between nerve cells might be directly controlled by genes, but
we have very little idea how higher functions such as language might be linked
to genes. The prevailing view is that the linkages are very indirect, and the
examples we have given show that developing cortical areas are very flexible
in the functional assignments they will accept.
Perhaps the most amazing example
of this comes from clinical observations on infants with intractable epilepsy
who have undergone removal of an entire cerebral hemisphere. One might expect
that this would completely block normal development, during which competing
language-related and other functions displace each other into opposite cerebral
hemispheres. (Thus the left hemisphere normally has a skeletal motor bias and
is optimized for speed, syntax, and visual details, whereas the right hemisphere
has a visceral motor bias and deals with large time domains, the prosody component
of language, and spatial relationship.) In defiance of all such predictions,
however, in children with one hemisphere removed, all of these operations can
collect and develop in the hemisphere that remains.
Adult Brains Can Change Their Nerve
Connections
Until recently, it was assumed
that brain cells and wiring change very little after puberty, when the final
form of the adult brain has taken shape. Thus many studies emphasized the slow
decay in cognitive function that frequently occurs in aging: loss of openness
to new experiences and so on. We still have to explain, however, why some people
can show striking recovery from brain damage and
why it is that if we put on eyeglasses that magnify or shrink the visual world
we perceive, our ocular reflexes and hand-eye coordination soon adapt as though
nothing had happened. Changes in the nerve cells that regulate these reflexes
in monkeys have been monitored, and brain imaging experiments in humans have
shown the posterior parietal cortex to be involved. Even
more striking, we can wear glasses that either turn our visual world upside
down or reverse left and right, and within a few days our perceptions change
so that we can function almost normally, even throwing and catching a ball.
(After we take off the glasses, it takes a day or more for appropriate function
to be restored.) It is difficult to reconcile these observations with the assumption
of a fixed adult structure.
***************
DESIGN NOTE: IMPORTANT POINT
Consider the intriguing case of
the woman who spoke both Italian and English and went to work as a United Nations
translator. Before she began her new job, her left hemisphere, the normal locus
of language, was used for both languages. After she had been in the job a few
months, Italian switched to the right hemisphere!
***************
Expansion and Contraction of Cortical
Areas
A large number of direct experiments
have now demonstrated that the adult cortex can remodel itself within localized
areas. There is debate over
whether these changes involve the actual growth of new axons and connections
over long distances, or whether existing horizontal connections between cortical
regions, normally silent, become active. Probably
both events occur. The most detailed work has been done in monkeys and entails
making direct electrical recordings from the somatosensory cortex. More recently,
imaging techniques have permitted similar observations in human brains. When
performance of a particular sensory or motor activity is emphasized (such as
reading Braille with one finger or developing a repetitive and skilled motor
activity with one finger), the portion of sensory and motor cortex devoted
to that activity expands. Conversely, when input from a digit is suppressed,
for example by taping one digit to the next, the area of cortex that usually
represents that digit is appropriated by adjacent digits. A similar phenomenon
occurs in the visual system. When a small area of the retina is damaged, the
area of visual cortex that represents that area is invaded by adjacent retinal
areas, a process called "filling in." This
is what normally happens with the blind spot on our retinas, a small area where
photoreceptors have been pushed aside by optic nerve fibers gathering to project
into the brain.
Brain changes that occur during
filling in or shifts in hand-eye coordination happen in only 10--30 seconds---much
too fast and far for new connections to grow. Changes that occur over periods
of days or weeks as new motor or sensory skills are acquired can involve distances
of more than a centimeter of cortex and may involve new growth of axons. The
ability of a cortical area that represents one of our fingers to either expand
or contract probably reflects a continuous competitive give and take between
neurons. If one neuron becomes much more active because it is needed for some
skilled task, it can begin to encroach on areas used by other neurons. If it
becomes more silent because fewer cells are talking to it, its sphere of influence
contracts. These changes might be of the sort shown in Figure 6-6, altering
the strength of existing synapses and/or forming new synapses. Such plasticity
enables us to adapt to and learn new situations.
A change in somatotopic organization
of the hand area in humans has been observed by means of magnetoencephalography
after surgical separation of webbed fingers (syndactyly). The
presurgical maps displayed shrunken and disordered hand representations. Within
weeks after surgery, the cortex had reorganized to reflect the functional status
of the newly separated digits. This finding is consistent with the results
of the experiment shown in Figure 6-7. The somatosensory cortex appears to
use the timing of arriving information to create spatial representations of
the fingers. Because input from one finger is usually synchronous and separate
from input from the other fingers, the cortical representation of that finger
is separate.
Blind people who read Braille literally
reconfigure sensory cortex for the fingertips. The area devoted to the finger
used for reading is several times larger than the corresponding area in sighted
people. The expansion of this area as Braille is learned can be followed in
imaging experiments. String players exhibit an increased cortical representation
of fingers of the left hand. During
the training of fingers to tap out a particular sequence, the area of primary
motor cortex activated by performing the sequence expands, and the changes
persist for several months. In
one experiment, one group of adults was given a daily five-finger exercise
to play, up and down a keyboard, and another group was told just to press the
keys randomly. The brain's representation of hand muscles in the subjects who
learned the piano exercise increased threefold compared with subjects who randomly
operated the keyboard. The biggest surprise came from subjects who were taught
the exercise but then told just to rehearse it mentally, not manually, while
looking at the keyboard. This mental exercise achieved the same result as manual
practice.
***************
DESIGN NOTE: IMPORTANT POINT
Mental rehearsal of a finger exercise
can increase the area of cortex that represents the hand just as effectively
as actual manual rehearsal can. This may be why imagining movement as a way
of learning and refining it has been developed into therapies for rehabilitation
and techniques for training of dancers and athletes.
***************
Cortical Plasticity and the Phantom
Limb Phenomenon.
Cortical plasticity appears to
play a central role in "phantom limb" phenomena observed after amputation
of an upper limb. Patients
experience sensations such as itch or pain in their no-longer-existent limb.
The invasion of an area of somatosensory cortex that had been responding to
a now-absent limb may underlie the sensations involved. The
amount of phantom limb pain correlates with the extent of neuronal reorganization
in the somatosensory cortexes. In
some patients who have undergone upper limb amputation, the face area invades
the area that had been responding to the limb. (The
area of cortex representing the face lies just next to the area representing
the limb; see Figure 3-6.) Stimulation of the face is then experienced as sensation
arising from the hand as well as from the face. A systematic, one-to-one matching
is reported between specific regions on the face and individual digits of the
hand. A drop of warm water allowed to trickle down the face is felt also as
warm water trickling down the phantom limb. In the case of an amputation just
above the elbow, stimulating either the face or the remaining upper arm can
cause feeling "in the fingers." This is presumably because in the
somatosensory body map, the hand area is flanked on one side by the face and
on the other by the upper arm and shoulder.
Another striking example of plasticity
after limb amputation is seen when a tall mirror is placed vertically on a
table and perpendicular to the patient's chest, so that a mirror reflection
of the normal hand is seen "superimposed" on the phantom. Moving,
touching, or vibrating the normal hand now causes a corresponding sensation
in the phantom hand, but heat, cold, and pain are not transferred. This suggests
that there is a normally latent link between brain areas in the right and left
cerebral cortexes representing the two hands whose activity can be brought
to awareness if visual input is provided. In some cases, viewing movement of
the mirror image relieves chronic spasms and pain in the phantom limb, perhaps
by providing sensory feedback for motor commands that usually register as pain
because they lack such feedback.
Social Experience Can Alter Brain
Structure
Given the plasticity of our sensory
and motor cortex, it would seem reasonable to look for plasticity in parts
of the brain that regulate our more complicated social and emotional behaviors.
Here there are very little data, apart from studies on behavioral effects of
impoverished early environments (these studies are mentioned in Chapter 7).
We know much less about the brain pathways underlying these more complex behaviors
than about more primary sensory and motor parts of the brain. Imaging studies
have shown complex changes in brain activity correlated with schizophrenia
and other psychopathologies, but interpretation of the data is in its infancy.
We are not yet able, for both ethical and practical reasons, to induce a behavior
change in human subjects (such as the change from a dominant to a submissive
personality) and then examine the effect on the activity of nerve cells in
the hypothalamus.
***************
DESIGN NOTE: IMPORTANT POINT
If the wiring of our adult sensory
and motor cortex can be altered by training, what about the parts of our brain
that control social and emotional behaviors?
***************
Animal studies, however, provide
evidence for a feedback loop between wiring of the adult brain and complicated
social behaviors. It is very likely that increasingly sophisticated imaging
techniques will yield similar information for humans. We would, in fact, expect
that as evolution worked at the group level of animals to shape their social
structure, brain plasticity appropriate for switching between alternative social
roles would have been generated. This is presumably because role specialization
increases the fitness of the whole group.
An example of such role specialization
comes from studies of an African cichlid fish species in which aggressive males
command large territories and keep other males at bay. These dominant males
have enlarged nerve cell bodies in the region of the hypothalamus that regulates
mating. If a dominant male is bullied by an even larger male, it becomes submissive
and the hypothalamus cells shrink along with the size of the testes, which
cease producing sperm. Dominant males have bright coloration unlike that of
females and subordinate males, so they are more susceptible to predation. When
a dominant male disappears, all the previously meek males rush into the area
and start fighting. The winner then grows bigger and gains bright coloration,
his hypothalamus cells and gonads enlarge, and sperm production begins.
Monitoring exactly how individual
nerve cells are changing when social experience alters behavior is very difficult
in vertebrate nervous systems, because these cells are extremely small and
numerous, and their anatomy is not well understood. It has been possible, however,
to take an analysis to the level of single nerve cells in studies on the invertebrate
crayfish, whose nerve cells are much larger. A neurotransmitter (serotonin),
which is known to be involved in the expression of aggression in many animals,
acts differently on a neuron that controls the escape reflex in dominant and
subordinate animals. This difference is due to a change in the postsynaptic
receptor molecules on which serotonin acts.
Most relevant to humans, of course,
are experiments on monkeys or apes. Numerous studies have documented neuroendocrine
changes that correlate with dominance or submission in these animals. Removal
of a dominant male usually results in competition, followed by behavioral changes
in the winner. In many mammals, high dominance status correlates with increased
adrenocorticosteroid levels. It
is likely that similar changes occur in humans: If we change our group role
either from "loser" to "winner" or from submissive to dominant,
long-term changes in brain wiring probably take place. The increasingly powerful
magnetic imaging techniques being developed may soon let us observe localized
brain changes that correlate with such events.
Limits of Brain Plasticity
What are the limits of the plasticity
of our brains? What can and what can't be changed? This is still unclear. The
picture that has emerged so far is of critical periods during development when
major pathways that regulate sensing and acting are laid down and can be modulated.
Then, in adult brains, there is an ability to fine-tune these pathways if sensory
or motor demands change. We don't yet have a link between direct observations
made on our brains and more complicated aspects of our personality. Effective
therapies exist for altering such things as sexual dysfunctions, panic, and
manic or depressed moods, but other attributes (such as sexual orientation)
are strongly resistant to change. Perhaps
the brain areas that regulate some behaviors are simply less plastic than the
areas in charge of others.
Memory Is a Form of Brain Plasticity
An obvious kind of plasticity in
our adult brains is revealed by our daily experience of remembering things---facts,
faces, contexts, and manual skills. Each memory we can access reflects changes
that have taken place in nerve connections in our brains. The remembering of
phone numbers, facts, and places---which can be very rapid and may require
only one exposure to the relevant item---seems likely to rely more on rapid
changes in the strength of existing nerve connections. The slow learning and
remembering of skills and procedures, such as your experience when you are
trying to improve your tennis game, appear to involve cellular mechanisms very
similar to those responsible for the plasticity discussed in previous sections. Nerve
cells actually make new connections. An avalanche of exciting new experiments
are documenting changes in gene expression and synaptic molecules that correlate
with memory formation, and several pharmaceutical companies are rushing to
use this information to develop memory-enhancing drugs.
A moment's reflection on our own
experience makes it clear that there are several different kinds of memory.
These memory types are common to mice and men and have been studied in both
species. Working memory is what we access for very recent events, where it
is appropriate for recall of these events to lapse after a short time. It is
what we use to remember a telephone number we have just looked up until we
finish dialing it. There is an important reason why most telephone numbers
have seven digits. We can hold in awareness, or short-term memory, approximately
seven chunks (meaningful units) of discrete information. About five seconds
per chunk is required to commit these units to longer-term memory (as in memorizing
a phone number). Regions of
the prefrontal cortex appear to be most heavily involved in working memory,
and different areas specialize in spatial locations, object identification,
and verbal memory.
***************
DESIGN NOTE: SELF-EXPERIMENT
Think about how long you remember
a phone number that you have just looked up and will not use again. This is
the duration of your short-term memory, or working memory.
***************
Long-Term Memory
The specifics of some of the events
held in working memory, if they are perceived as important, might be passed
on to one of the two major kinds of long-term memory displayed by animals:
procedural memory and episodic memory. Procedural memories are the "recall" components
of learned action patterns. They preserve general principles for action and
ignore situation-specific details. Episodic memory refers to our ability to
recall specific places, facts, number, or instances. Procedural memory and
episodic memory involve different neural mechanisms. Birds can lose their songs
(a procedural memory system) if lesioned in one part of the brain, and they
can lose their ability to hide and relocate food (an episodic memory system)
if lesioned in another. Some human amnesiacs can learn new motor skills (procedural
memory) with no recall of having learned them (episodic memory). Other names
are also used for these two kinds of memory: noncognitive versus cognitive,
nondelarative versus declarative, implicit versus explicit.
We will deal here with only a few
of the different memory systems. At least six such systems can be distinguished
and associated with different brain structures: (1) Episodic memory (sometimes
referred to as explicit memory), the conscious recall of facts and events,
is associated with medial temporal lobe and diencephalic structures. (2) Working
memory, which is discussed in Chapter 12, is associated with prefrontal cortex.
(3) Priming, which relates perceptual and conceptual representations, is associated
with occipital, temporal, and frontal cortex. (4) Motor skill learning is associated
with the striatum. (5) Classical conditioning, wherein we learn relationships
between perceptual stimuli and skeletal motor responses, is associated with
the cerebellum. (6) Emotional conditioning, which relates perceptual stimuli
and emotional responses, is associated with the amygdala.
Episodic, or explicit, memory consists
of our ability to recall specific places, facts, numbers, or instances (as
discussed above). Some restrict
episodic memory to the recall of events that happened to the individual and
use semantic memory for recall of facts such as the location of cities. Several
recent studies have suggested that the hippocampus and other parts of the brain
play a role in the transfer of information from working, or short-term, memory
to this kind of long-term memory. If
the hippocampus is damaged (by anoxia or mechanical shock) or is removed, the
ability to form new memory is lost. Work with many patients has shown that
it is possible for acquisition of long-term memory to be lost completely, while
all other intellectual powers remain intact. These subjects can read a newspaper,
understand all its contents, and 20 minutes later have no recall of having
done so. The kind of memory required to learn both mental and physical skills
(procedural memory) remains intact. Furthermore, there is no damage to the
working memory used in immediate recall.
Patients with bilateral damage
to the amygdala but with intact hippocampus cannot acquire conditioned autonomic
responses (such as a skin conductance response to a color that has been paired
with an unpleasant noise), but they can recall the pairing of the conditioned
and unconditioned stimuli. Conversely, patients with intact amygdala but bilateral
damage to the hippocampus learn the autonomic conditioned response without
grasping the facts about the conditioning stimuli. The
storage of both explicit factual memories and emotional memories involves the
medial temporal lobe as well as frontal and other areas. Imaging studies show
that activity not just in the hippocampus portion of the medial temporal lobe,
but also in a surrounding area called the parahippocampal cortex, correlates
with whether novel items are remembered. Imaging studies further suggest that
memory storage processes involving words are associated with enhanced activity
in the left prefrontal cortex, whereas the right hemisphere becomes more active
when visual images are involved. Memory retrieval is accompanied by enhancement
of right prefrontal activity. Both imaging and brain lesion studies suggest
that memory retrieval is under the executive control of the prefrontal cortex.
***************
DESIGN NOTE: IMPORTANT POINT
Damage to the hippocampus can abolish
explicit recall, whereas damage to the amygdala can abolish emotional memory.
The idea is that our hippocampus and adjacent structures link the separate
parts of a long-term memory as they are formed, making it possible for all
to be evoked when the memory is recalled.
***************
A famous example of a complex memory
occurs in Marcel Proust's novel Remembrance of Things Past. It is the flood
of recollections stimulated by eating a small, rich pastry called a madeleine. The
event being recalled originally started with perception: the narrator's feeling
and seeing his cup of tea, the spoonful he raised to his lips, along with other
visual, olfactory, and motor qualities engaging different parts of the cortex.
These would have passed their sensations to the hippocampus, and the hippocampus
would then have orchestrated the formation of an associative net linking all
the perceptions into a multifaceted experience. At a later time, reenacting
just one of the events of this scene (eating the madeleine), like pulling a
single strand of the net, would draw up behind it all the other strands with
which it is connected. Figure 6-8 may help you visualize what may be going
on here.
Providing enough cells in the hippocampus
to support forming new memories may require the violation of a long-standing "law" about
brain cells: that in the adult human brain they do not divide. Division of
cells in the hippocampus has recently been observed for the first time, even
in aged adults. It has also
been discovered that the decay of memory abilities observed in patients with
Alzheimer's dementia correlates with MRI measurements showing a decrease in
the size and volume of the hippocampus.
Figure 6-8
Model of the role of the hippocampus
in forming memories. (a) Features of a scene such as taste, vision, and emotional
feeling---processed in different areas of the cortex---all send signals to
the hippocampus. (b) Networks of nerve cells in the hippocampus reassociate
the separate features and send signals back to the cortex. (c)
As a result, the areas of the cortex become linked in such a way as to form
a long-term memory that unites the separate features of the scene.
Researchers have measured the activity
of the hippocampus in lab rats while the rats are exploring and learning a
new environment. Simultaneous recordings from 100 or more nerve cells show
that their firing patterns correlate with the position of the animal and that
these firing patterns change when the animal's position changes. Even
more interesting, the correlated activity of the cells during sleep sometimes
repeats the activity of those cells during earlier spatial exploration. This
may reflect memory consolidation of the exploration. A role for the hippocampus
in mice learning their way around mazes is suggested by "knockout" experiments
that use genetic manipulations to delete specific synaptic components in the
hippocampus. In mice with such
deletions, learning is compromised. Brain imaging studies in humans have now
shown that locating and navigating accurately in a virtual-reality town presented
by a computer display are associated with activation of the right hippocampus.
Why do we not remember events before
we were 3 or 4 years old? Studies on children show that from the time they
begin to talk, at around age 2, they have both generic memory (recall of repeated
episodes) and episodic memories (recall of single episodes). Amygdala and hippocampus
have developed sufficiently to support emotional and factual memories. But
the kinds of memories that last a lifetime are initiated only when children
begin to weave together autobiographical memory---a story line---at around
age 3 1/2 .
It is at this same age that children begin to show strikingly different approaches
to their daily experience, different ratios of introversion/extraversion, and
patterning versus dramatic behaviors.
Memory is not like a fixed filing
system. It is not recording information like a camera. What is created is a
semblance or approximation of the original events, sometimes with many biases
and errors. We know too that the strands of memory are not complete, much information
is filtered out. The strands are not always accurate; they can be distorted
by personal goals, current knowledge, or social conventions. A
given memory changes over time to resemble previous experiences of a similar
nature, corresponding to the mental templates into which we fit our experiences.
Numerous experiments demonstrate that false memories do indeed occur.
***************
DESIGN NOTE: SELF-EXPERIMENT
You can perform a demonstration
of false memory by simply reading out loud to a friend a list of similar items
(such as bed, rest, awake, tired, dream, wake, snooze, doze, slumber). If you
then ask your friend whether an unspoken but related word (such as sleep) was
on the list, he or she is very likely to report that it was there, even though
it was not.
***************
Models of Recognition and Memory
Models of interactions between
cortex and hippocampus during recognition and memory have been constructed
by using computer nerve nets that are very simplified versions of systems of
real neurons. A nerve net that
models a first-stage attentional subsystem (like the hippocampus) learns and
forms short-term memory traces that are relayed to a second stage (like the
medial temporal lobe), where long-term traces are formed. These are relayed
back to the first stage. Learning occurs when a mismatch between bottom-up
and top-down patterns occurs. Thus seeing a familiar face does not trigger
learning (that face is already present in the top-down patterns), but seeing
an unfamiliar face does. Efforts are being made to correlate such nerve net
models with brain imaging experiments. Activation of left dorsal frontal, hippocampal,
and other medial temporal brain areas is observed during the encoding of words,
whereas the encoding of unfamiliar faces activates corresponding areas in the
right hemisphere.
Imaging studies are demonstrating
that our learning and memory engage areas of the cortex that deal with sensory
input and motor output. Anatomically
separable regions in the left hemisphere tend to process words for distinct
kinds of items, such as animals, persons, or tools. At least 15-20 different
categories for storing knowledge have emerged from brain lesion studies, the
lesions being spread mainly over the occipitotemporal axis of the left temporal
lobe. Among the categories
are plants, animals, body parts, colors, numbers, letters, nouns, verbs, proper
names, faces, facial expressions, and categories of foods such as fruits and
vegetables, and they all seem to have separate visual and verbal storage areas.
The category an object belongs to acutely affects how it registers in the brain.
***************
DESIGN NOTE: IMPORTANT POINT
In thinking about a cow, we apparently
must use the circuitry for the category "animal" in order to come
up with a color, size, and so on. Objects in a different category, such as "fabricated
objects" can pass through a different set of processing channels.
***************
Work with amnesiacs suggests that
parallel brain systems exist for remembering specific items and remembering
the categories to which they belong. In
some amnesiac patients, if a series of related items are displayed, knowledge
of the relationship is formed by some sort of procedural memory process, but
recall of specific items is impaired. Thus an item might not be remembered,
but it can be assigned to a category. This suggests that the neocortex can
gradually acquire classification knowledge independently of the hippocampus
and related bodies that are damaged in amnesia.
One study on a patient who had
sustained cerebral damage shows evidence for (1) a major division between visual
and linguistic higher-level representations and (2) processing subsystems within
language. The patient could not name animals, regardless of the type of presentation
(auditory or visual), but had no difficulty naming other living things and
objects. Accuracy of the physical attributes of animals could be distinguished
(such as whether animals were correctly colored), but the color of a given
animal could not be stated. In this case, knowledge of physical attributes
was strictly segregated from knowledge of other properties in the language
system. In other cases, patients
are unable to generate visual images "in the mind's eye" but have
reasonably intact recognition of what they see. The opposite is also observed:
Recognition is impaired but internal imagery is intact. This observation suggests
that functionally (and perhaps anatomically) distinct routes to a central store
of visual templates can be selectively damaged.
We have talked about changes in
nerve nets, areas becoming linked, and regions where information is stored,
but in this book we are not examining the details of what goes on at the level
of individual nerve cells and the synapses they use to "talk" with
each other. Most investigators assume that memories ultimately have to correspond
to long-term changes, either strengthening or weakening, in the information
transmitted by individual synapses. They probably also involve both the formation
of new synapses and the destruction of existing ones (as in Figure 6-6), processes
central to the development and wiring of brain regions described earlier in
this chapter. An enormous amount of contemporary research is focused on trying
to describe the cellular mechanisms that can cause such changes. There is now
evidence that nearly every aspect of synaptic function can be altered in a
long-term way: how much neurotransmitter is released when an impulse reaches
a presynaptic terminal;the sensitivity or number of postsynaptic receptor molecules
that are activated by the neurotransmitter; and the tightness and surface area
of the synaptic contact. Formation of new synapses during memory consolidation
has also been documented. In many of these cases, the neurotransmitter glutamic
acid and its several postsynaptic receptors appear to play a central role.
Procedural Memory
The formation of our procedural,
implicit, or nondeclarative memories and habits are associated with regions
of the cortex, thalamus, and basal ganglia that are largely distinct from those
involved in the formation of explicit memories. This
system can sometimes step in to replace functions that a damaged explicit memory
system can no longer serve. Procedural
memory is used in learning complicated motor sequences associated with manual
skills, and as we noted earlier, plasticity in the adult brain is associated
with such learning. For example, when a novel finger exercise is taught to
the right hand, imaging studies show increased activity in left motor, premotor,
supplementary motor, and sensory cortex and in the right anterior lobe of the
cerebellum. The idea is that the initial stages of motor learning are related
to somatosensory feedback processing and internal language for guidance of
the finger movements. As skill is acquired, the areas of activation become
less global.
PET imaging studies on the processes
underlying procedural memory have made use of the phenomenon of priming, a
change in the ability to identify or produce an item as a result of a specific
prior encounter with it. A
standard procedure is to show, on a screen, during the hour before a conversation
with the subjects, a word or picture for which there is no conscious recall,
and then ask subjects to say the first word that comes to mind when a list
of approximately ten word beginnings appears on the screen. For "mot-," for
example, the subject might reply "motor" or "mottle" or "motive." Those
who have seen the word "motel" on their screen within the past 30
minutes recall it without knowing why. When they are asked just to finish the
word, the visual cortex lights up, so the process seems more like perception
than thinking. This suggests little understanding of the word, only a perception
of its letter shapes. Patients with a damaged hippocampus perform this task
normally. By contrast, asking subjects to try to recall, from a previously
presented list, words that match the stem currently being presented causes
the frontal lobe to light up, which implies that conscious, higher-level thinking
is needed in the memory search. The simplest tasks that can be devised light
up several parts of the brain at once, which suggests many little "processors" or
agents that are linked together.
Olfactory Memories
Smell is one of our most powerful
and primitive memory systems. You
may have noticed this when a smell distinctive of your childhood unleashed
a flood of memories. Olfactory input links directly to primitive brain centers
in the hypothalamus, and manipulation of this system is the goal of a new aromatherapy
industry that aspires to influence mood through smells, with different odors
facilitating alert, calm, or refreshed moods. In
addition to the primary olfactory system that responds to smells, higher vertebrates,
including humans, contain a second system, the vomeronasal system, that responds
to sexual attractant molecules (pheromones). Although this system is very important
in the mating of many mammals, it has been assumed to be vestigial in humans.
But perhaps this is not so. The vomeronasal system does project to regions
of the hypothalamus that are involved in sexual and affective behavior. And
only recently it has been found that odorless compounds from the armpits of
women in the late follicular phase of their menstrual cycles can shorten the
menstrual cycles of women exposed to the compounds. Some biotechnology companies
are now working on what they think are pheromones extracted from human skin
that can regulate affect. Another
random and curious point about what may be a genetically encoded smell memory:
A woman, when asked to sniff T-shirts that men have slept in, tends to prefer
the smells emanating from men who have histocompatibility complexes (genes
involved in generating our immune systems) that differ from her own. Mating
with such men would confer a wider array of immunity options on the offspring.
The Sexual Brain---Plasticity Induced
by Hormones
This chapter has emphasized how
malleable the brain is to shaping by the external environment. A final example
of this plasticity is a topic that has inspired much debate: the sexual differentiation
of our brains. A crucial environment during the brain's plastic development
is the uterus, where the developing embryo is exposed not only to its own hormones
but also to those of adjacent embryos and its mother. This environment shapes
the development of sexually differentiated brains and behaviors. There is intense
interest in this area, and few topics excite livelier debate than the issue
of nature versus nurture in determining sexual behaviors.
After the internal and external
genitalia, the brain is the most significant area of sexual differentiation. The
hypothalamus contains separate centers for male-typical and female-typical
sexual behavior and feelings. The medial preoptic area (just in front of where
our optic nerves cross each other) plays a vital role in male-typical sexual
behavior. It has a high level of receptors for testosterone (released by the
gonads). Damage to this region in male animals of many species can cause a
reduction in or cessation of heterosexual copulatory behavior and sometimes
causes those males to perform more female-typical behaviors in approaches to
a stud male. If this area in normal male animals is electrically stimulated,
they begin mounting and pelvic-thrusting behaviors. At least one cluster of
nerve cells in the medial preoptic region is sexually dimorphic---that is;
it differs between the sexes. The third interstitial nucleus of the anterior
hypothalamus is threefold larger, on average, in males than in females. This
is the area that has been suggested to vary with sexual orientation in males,
being smaller in gay men. The
formation of the sexually dimorphic nucleus depends crucially on the circulating
levels of testosterone during a critical period just prior to and just after
birth. During this period in females, neurons of the nucleus die, and this
can be prevented by adding testosterone. It takes a specific external signal,
the presence of sufficient circulating levels of androgens, to reprogram development
in the male direction.
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DESIGN NOTE: IMPORTANT POINT
Androgen receptors are found throughout
the brain, and their stimulation by testosterone during development appears
to play a large part in superimposing male features on the brain's intrinsic
female developmental program.
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Two further brain regions that
show sexual dimorphism are the corpus callosum and the anterior commissure.
The anterior commissure is a bundle of nerve fibers connecting the two hemispheres
that appeared early in vertebrate evolution; the larger corpus callosum that
connects the hemispheres is unique to placental mammals. Both of these structures
have been reported to be a larger part of the total brain in women than in
men, which suggests richer connectivity between the hemispheres in women. This
difference may account for women's greater verbal fluency and for the fact
that language seems to be restricted to the left hemisphere to a lesser extent
in women than in men. A number of other differences between men and women in
brain organization have been suggested. Brain
damage studies show that for language and control of hand movements, women
depend more than men on anterior regions of the brain.
Hormonal Influences on Behavior
The organizing effects of testosterone
have major consequences for behavior. Prenatal testosterone levels in male
monkeys influence their levels of rough-and-tumble play. Human girls who have
congenital adrenal hyperplasia, and thus are exposed to unusually high androgen
levels prenatally, can show play and toy preferences more typical of males.
There is considerable variability in sexual behavior even among animals of
the same sex, and this can sometimes be traced to natural processes during
development. Female rats sometimes mount other females and perform pelvic thrusting.
The propensity for this male-typical behavior is strongly influenced by the
position of the female when it was a fetus in the uterus. Female fetuses that
happen to lie between male fetuses are more likely to display mounting behavior
as adults than those that lie between female fetuses. This appears to be because
they take up testosterone from the adjacent male fetuses. In human female-to-male
transsexual operations with testosterone administration, aggressive tendencies,
sexual motivation, arousability, and visuospatial ability increase and verbal
fluency declines. The results for male-to-female subjects after androgen deprivation
are changes in the opposite direction.
A masculinizing effect can be seen
on the auditory systems of women who have a male twin. Normal
human cochleas (inner ears) generate very weak sounds that propagate back through
the middle ear, where they can be recorded. Women exhibit more of these weak
sounds than men, a sex difference that exists from birth. Females who have
a male twin generate about half the average number of sounds observed in same-sex
female twins and in female non-twins, about the same number as seen in men.
Prenatal exposure to high levels of androgens has apparently had a masculinizing
effect on the auditory systems of these women.
The trait of male aggressiveness
in mammals correlates with greater levels of testosterone from puberty onward.
Males castrated before puberty (including human eunuchs) are more docile. The
relationship between testosterone and behavior is not a simple one, for testosterone
and its related group of androgens can be both causes and effects of aggressive
behavior. Nothing is ever simple when we are dealing with hormones, and the
testosterone = aggression equation is no exception. Deficiency of testosterone
can also be linked to aggression. (Targeted
at men over age 50 who worry about their declining energy and libido, an "Androderm
patch" sold by a pharmaceutical company releases 5 mg a day of testosterone
into the bloodstream. It is reported to boost libido, increase muscle mass,
and lower the voice! There are concerns, however, about the long-term effects
of such hormone therapy.)
***************
DESIGN NOTE: IMPORTANT POINT
The greater aggressiveness of human
males is perhaps the most striking example of a sexually differentiated trait.
The trait is observed in most mammals and is presumably the result of sexual
selection during evolution.
***************
The amygdala is important in sexual
behavior and aggressive behavior, which involve the corticomedial and basolateral
nuclei, respectively. The corticomedial nucleus links to the medial preoptic
area, and a corticomedial lesion can interfere with sexual behavior. The basolateral
nucleus connects to regions farther back in the hypothalamus that play a role
in aggressive behavior, and a basolateral lesion can reduce aggressive behavior
and rough-and-tumble play. Bilateral ablation of the amygdala has been performed
on very aggressive adults and children who have not responded to other forms
of treatment, with the result of reducing their aggressive behavior.
Hormonal Influences on Visuospatial
Skills
The other most widely studied difference
between male and female brains involves spatial or visuospatial skills. On
average, males (rat or human) are better at mazes than females, and human males
are better at visualizing rotating objects. (We don't know how to test rats
for this latter capability!) Conversely, women tend to outperform men on some
tests of verbal ability and fluency. Human women (and female rats) have a greater
tendency to use landmarks in spatial learning tasks, whereas males use geometric
cues. Are these cognitive differences inborn or learned? Probably both, but
it is striking that women who were exposed to high levels of androgenizing
hormones while they were fetuses (either as a result of congenital adrenal
hyperplasia or because their mothers were given the synthetic steroid diethylstilbestrol)
score better than other women on spatial tests. Similarly, the maze-running
performance of female rats given androgens around the time of birth is better
than that of untreated females. In androgen-insensitivity syndrome, chromosomal
males have testes that secrete testosterone, but these males have a mutation
in the gene for the androgen receptor. The body acts as though no androgens
were present and develops as female; individuals usually are raised as girls.
They do worse on visuospatial tasks than their male relatives and have verbal
skills similar to their female relatives. During the menstrual cycle in women,
as estrogen levels increase, spatial abilities decrease, and articulatory abilities
increase. In men, a lowering of testosterone levels in the spring correlates
with an increase in spatial abilities. In all of these examples, hormones apparently
modulate the synaptic pathways that underlie our higher cognitive faculties.
***************
DESIGN NOTE: IMPORTANT POINT
Cognitive patterns may remain sensitive
to hormonal fluctuations throughout life. Recent animal studies have shown
that steroid hormones can cause cellular changes and synaptic reorganization
in the adult hypothalamus. Estrogen
administration stimulates memory and the growth of axons and dendrites in the
hippocampus.
***************
Summary
The examples of brain plasticity
that have emerged from studies on the sexual differentiation of the brain and
on the mechanisms of learning and memory paint a picture of our developing
and adult brains as plastic devices that are constantly re-forming themselves.
The evolutionary rationale for this plasticity is that it permits us to wire
up our brain circuits in response to the world in which we actually grow up
and function, rather than the world of our ancestors. This description represents
a revolutionary change in perspective, for as recently as 30 years ago, it
was widely assumed that development was rigidly programmed and that adult brains
remained constant through life. At the level of individual cells and complex
systems of cells, what we see instead is a constant testing of what works best
and an ability to overcome even extraordinary perturbations or lesions in normal
development. A most dramatic example is provided by the near-normal development
of human infants that have had an entire cerebral hemisphere removed. We will
consider some further examples of brain plasticity when, in Chapter 11, we
discuss the effects of genetic mutations and brain lesions on the development
of areas of the brain crucial to language.
Each of our systems, from fundamental
visual and motor mechanisms to the higher functions of socialization and personality
formation, appear to have a critical period, or window of time, during which
their habits are laid down. Once the structures are formed, we are pretty much
stuck with them. Even so, our adult brains have abilities to rewire themselves
when new tasks of discrimination are required or when areas of brain tissue
have been damaged. Changes in the brains of some animals have been observed
to accompany changes in social status, and it is not unreasonable to suppose
that analogous processes might occur in humans. Subtle changes in nerve connections
underlie the memory systems that permit us to recall places and events and
to remember skilled action sequences. Interactions with the internal hormonal
environment also pattern brain plasticity, as in the sexual differentiation
of the brain. The immersion of each of our developing brains in a particular
physical, linguistic, and cultural environment generates in each case a physically
unique structure. This structure, broadly similar in all humans but differing
for each individual in the details, supports the generation and definition
of the human selves that are the subject of Chapter 7.
Questions for Thought
1. Permitting a nervous system
to wire up in a flexible way, depending on the environment that the organism
actually encounters, seems like such a good trick that one might expect animals
less able to do this, such as insects, to have lost out in the evolutionary
competition. Why, then, are beetles perhaps the most varied and numerous animal
species on this planet?
2. There is debate about whether
complicated nerve circuits---such as those that coordinate hand and eye movements---are
formed by processes akin to Darwinian evolution or by an active, constructive
learning process. Are the nerve pathways selected from existing options or
invented? Can you design some thought experiments that would determine whether
either of these alternatives (or both) is (or are) correct?
3. Suppose you were curious about
observing the plasticity of your own adult cerebral cortex, and suppose you
had a friend who was willing to let you play with her MRI or magnetoencephalography
equipment. This machinery allows you to observe what brain areas become most
active during a given task. What experiment would you design, and what result
might you expect to see?
4. Storage in memory of the objective
factual components and the emotional components of an experience appears to
require the activities of two different brain structures. What are these structures,
and what kinds of observations have demonstrated their importance?
Suggestions for Further General
Reading
Deacon, T.W. 1997. The Symbolic
Species: The Co-Evolution of Language and the Brain. New York: Norton. Chapters
6 and 7 discuss brain development and its plasticity.
Bear, M., Connors, B., & Paradiso,
M. 1996. Neuroscience: Exploring the Brain. Baltimore, MD: Williams & Wilkins.
Chapter 18 of this book discusses the wiring of the brain.
Schacter, D.L. 1996. Searching
for Memory: The Brain, the Mind and the Past. New York: Basic Books. An engaging
description of memory mechanisms and how they can be distorted.
LeVay, S. 1993. The Sexual Brain.
Cambridge, MA: M.I.T. Press. This book is one of the sources for the section
on the sexual differentiation of the brain.
Reading on More Advanced or Specialized
Topics
Deacon, T.W. 1990. Rethinking mammalian
brain evolution. American Zoologist 30:629--705. This article summarizes the
experiments, described in Figure 6-5, that demonstrated that cortical function
can be switched from one sensory mode to another.
Florence, S.L., Jain, N., Pospichal,
M.W., Beck, P.D., Sly, D.L., &Kaas J.H. 1996. Central reorganization of
sensory pathways following peripheral nerve regeneration in fetal monkeys.
Nature 381:69--71. This is the article on which Figure 6-7 is based.
Yeh, S., Fricke R., & Edwards
D. 1996. The effect of social experience on serotonergic modulation of the
escape circuit of crayfish. Science 271:366--369. These experiments demonstrate
a link between social experience and the chemistry of specific synapses.
Milner, B., Squire, L.R., & Kandel
E.R. 1998. Cognitive neuroscience and the study of memory. Neuron 20:445--468.
A description of the history and current status of studies on the mechanisms
of memory.
Ungerleider, L.G. 1995. Functional
brain imaging studies of cortical mechanisms for memory. Science 270:769--775.
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