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Science Brain and Behavior contiuned 19

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HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 191
to be true. Even with the development of the microscope,
the appeal of preformation proved so
strong that biologists claimed to see microscopic
horses in horse semen.
By the middle of the nineteenth century, the
idea of preformation began to wane as people realized
that embryos look nothing like the adults
that they become. In fact, it was obvious that the
embryos of different species more closely resemble
one another than their respective parents.
Figure 6-3 shows the striking similarity in the
early embryos of species as diverse as salamanders,
chickens, and humans.
Early in development, all vertebrate species
have a similar-looking primitive head, a region
with bumps or folds, and all possess a tail. Only
as an embryo develops does it acquire the distinctive
characteristics of its species. The similarity
of young embryos is so great that many
nineteenth-century biologists saw it as evidence
for Darwin’s view that all vertebrates arose from
a common ancestor millions of years ago.
Although the embryonic nervous systems
are not shown in Figure 6-3, they are as similar
structurally as their bodies. Figure 6-4 details the
three-chambered brain of a young vertebrate embryo: forebrain, midbrain, and hindbrain.
The remaining neural tube forms the spinal cord. How do these three regions
develop? We can trace the events as the embryo matures.
Gross Development of the Human Nervous System
When an egg is fertilized by a sperm, the resulting human zygote consists of just a
single cell. But this cell soon begins to divide, and by the 15th day, the emerging
embryo resembles a fried egg, as shown in Figure
6-5. It is made of several sheets of cells with
a raised area in the middle called the embryonic
disc, which is essentially the primitive body.
By day 21, 3 weeks after conception, primitive
neural tissue, known as the neural plate, occupies
part of the outermost layer of embryonic cells.
The neural plate first folds to form the neural groove, as detailed in Figure 6-6. The neural
groove then curls to form the neural tube,much as a flat sheet of paper can be curled
to make a cylinder.
Salamander Chick Human Figure 6-3
Embryos and Evolution
The physical similarity of
embryos of different species
is striking in the earliest
stages of development, as
these salamander, chick,
and human embryos show.
This similarity led to the
conclusion that embryos are
not simply miniature versions
of adults.
Brainstem
Head
Body
Forebrain
Midbrain
Hindbrain
Neural tube
(forms spinal
cord)
Figure 6-4
Basic Vertebrate Nervous System
Forebrain, midbrain, and hindbrain are
visible in the human embryo at about 28
days, as is the remaining neural tube,
which will form the spinal cord.
Prenatal Stages
Zygote ! fertilization to 2 weeks
Embryo ! 2 to 8 weeks
Fetus ! 9 weeks to birth
Day 1: Fertilization Day 2: Division Day 15
Embryonic
disc Figure 6-5
From Fertilization to Embryo Development begins at fertilization
(day 1), with the formation of the zygote. On day 2, the zygote begins to
divide. On day 15, the raised embryonic disk begins to form. Adapted from
The Developing Human: Clinically Oriented Embryology (4th ed., p. 61), by K. L. Moore,
1988, Philadelphia: Saunders.
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Micrographs of the neural tube closing in a mouse embryo can be seen in Figure
6-7. The cells that form the neural tube can be thought of as the “nursery” for the rest
of the nervous system. The open region in the center of the tube remains open and matures
into the brain’s ventricles and the spinal canal.
The body and the nervous system change rapidly in the next 3 weeks of development.
By 7 weeks (49 days), the embryo begins to resemble a miniature person. Figure
6-8 shows that the brain looks distinctly human by about 100 days after conception,
but it does not begin to form gyri and sulci until about 7 months. By the end of the 9th
month, the fetal brain has the gross appearance of the adult human brain, even though
its cellular structure is different.
Another developmental process, shown in Figure 6-9, is sexual differentiation.
Although the genitals begin to form in the 7th week after conception, they appear identical
in the two sexes at this early stage. There is not yet any sexual dimorphism, or structural
difference between the sexes. Then, about 60 days after conception, male and
female genitals start to become distinguishable.
What does sexual differentiation have to do with brain development? The answer is
hormonal. Sexual differentiation is stimulated by the presence of the hormone testosterone
in male embryos and by its absence in female embryos.
Testosterone changes the genetic activity of certain
cells,most obviously those that form the genitals, but neural
cells also respond to this hormone, and so certain regions
of the embryonic brain also may begin to show sexual
dimorphism, beginning about 60 days after conception.
Prenatal exposure to gonadal hormones acts to shape
male and female brains differently because these hormones
activate different genes in the neurons of the two sexes. As
we shall see, experience affects male and female brains differently;
therefore genes and experience are shaping the
brain very early in life.
192 ! CHAPTER 6
Neural
plate
Neural
groove
21 days
Neural plate
(primitive 18 days neural tissue)
Neural groove
(closing to form
neural tube)
Neural tube Ventricle
22 days
Developing
forebrain
Developing
heart
Neural
tube
24 days
Anterior neural
folds (close to
form brain)
Neural tube
23 days
Figure 6-6
Neural Tube Forms A long depression,
the neural groove, first forms in the
neural plate. By day 21, the primitive
brain and neural groove are visible. On
day 23, the neural tube is forming as the
neural plate collapses inward along the
length of the dorsal surface of the
embryo. The embryo is shown in a
photograph at 24 days.
SPL/CMSP
(A) Day 9 (B) Day 10 (C) Day 11
Figure 6-7
Neural-Tube Development Scanning
electron micrographs show the neural
tube closing in a mouse embryo.
Reproduced with the permission of Dr. R. E.
Poelman, Laboratory of Anatomy, University of
Leyden.
Visit the Brain and Behavior Web site
(www.worthpublishers.com/kolb)
and go to the Chapter 6 Web links to
view images of human embryos at various
stages of development.
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HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 193
25 days 35 days 40 days 50 days 100 days
8 months
9 months
5 months
6 months
7 months
Urogenital
membrane
Anal
membrane
Indifferent stage
Developing
penis
folds
Penis
Scrotum
Urethral
Scrotal
folds
Anus
Developing male genitalia
Anus
Clitoris
Labial
folds
Developing female genitalia
Developing
clitoris
Anus
Anus
Labial
folds
Figure 6-8
Prenatal Brain Development The
developing human brain undergoes a
series of embryonic and fetal stages. You
can identify the various nervous system
parts by color (review Figure 6-4) as
they develop in the course of gestation.
Adapted from “The Development of the Brain,”
by W. M. Cowan, 1979, Scientific American,
241(3), p. 116.
Figure 6-9
Sexual Differentiation in the Human
Infant Early in development
(indifferent stage), male and female
human embryos are identical. In the
absence of testosterone, the female
structure emerges (left). In response to
testosterone, the genitalia begin to
develop into the male structure at about
60 days (right). Parallel changes take
place in the embryonic brain in response
to the absence or presence of
testosterone.
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Origins of Neurons and Glia
The presence of neural stem cells lining the neural tube, the nursery for the brain, has
only recently been confirmed in adults. The stem-cell layer is identified as a region,
from two to three cells thick, immediately adjacent to the ependymal lining of the lateral
ventricles (see a review by Morshead & van der Kooy, 2004).
A stem cell has an extensive capacity for self-renewal. It divides and produces two
stem cells, both of which can divide again. In adulthood, one stem cell dies after division,
leaving a constant number of dividing stem cells. In an adult, the neural stem cells
line the ventricles and thus form what is called the ventricular zone.
If lining the ventricles were all that stem cells did throughout the decades of a
human life, they would seem like odd kinds of cells to possess. But stem cells have a
function beyond self-renewal: they give rise to so-called progenitor cells (precursor
cells). These progenitor cells also can divide and, as shown in Figure 6-10, they eventually
produce nondividing cells known as neuroblasts and glioblasts. In turn, neuroblasts
and glioblasts mature into neurons and glia. Neural stem cells, then, give rise
to all the many specialized cell types in the central nervous system.
Sam Weiss and his colleagues (1996) discovered that stem cells remain capable of
producing neurons and glia not just into early adulthood but even in an aging brain.
This important discovery implies that neurons that die in an adult brain should be replaceable.
But neuroscientists do not yet know how to instruct stem cells to carry out
this replacement process.
One possibility is to make use of signals that the brain normally uses to control
stem-cell production in the adult brain. For example, when female mice are pregnant,
the level of the neuropeptide prolactin increases, and this increase stimulates the brain
to produce more neurons (Shingo et al., 2003). Perhaps these naturally occurring hormonal
signals will provide a way to replace lost neurons in the injured brain.
An important question in the study of brain development is how undifferentiated
cells are stimulated to form stem cells, progenitor cells, neuro- and glioblasts, and finally
neurons and glia. In other words, how does a stem cell “know” to become a neuron
rather than a skin cell? Recall from Chapter 3 that each human cell has 23 chromosome
pairs containing the approximately 20,000 genes of the
human genome. In each cell, certain genes are “turned
on” by a signal, and those genes then produce a particular
cell type.
“Turned on” means that a formerly dormant gene
becomes activated, which results in the cell making a
specific protein. You can easily imagine that certain
proteins are needed to produce skin cells,whereas other
proteins are needed for neurons. The specific signals for
turning on genes are largely unknown, but these signals
are probably chemical.
Thus, the chemical environment of a cell in the
brain is different from that of a cell that forms skin, and
so different genes in these cells are activated, producing
different proteins and different cell types. The different
chemical environments needed to trigger this cellular
differentiation could be caused by the activity of other
neighboring cells or by chemicals, such as hormones,
that are transported in the bloodstream.
You can see that the differentiation of stem cells
into neurons must require a series of signals and the
194 ! CHAPTER 6
Neural stem cell. A self-renewing,
multipotential cell that gives rise to any of
the different types of neurons and glia in
the nervous system.
Ventricular zone. Lining of neural stem
cells surrounding the ventricles in adults.
Progenitor cell. Precursor cell derived
from a stem cell; it migrates and produces
a neuron or a glial cell.
Neuroblast. Product of a progenitor cell
that gives rise to any of the different types
of neurons.
Glioblast. Product of a progenitor cell
that gives rise to different types of glial
cells.
Self-renewal
Progenitor
produced
Neuroblasts
and glioblasts
produced
Neurons
and glia
differentiate
Neural Glial
Stem
Progenitor
Blast
Specialized
Projecting
neuron
Interneuron Oligodendroglia Astrocyte
Cell type Process
Figure 6-10
Origin of Brain Cells Cells in the brain
begin as multipotential stem cells, which
develop into precursor cells, which
produce blasts, which finally develop
into specialized neurons or glia.
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HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 195
resulting activation of genes. A chemical signal must induce the stem cells to produce
progenitor cells, and then another chemical signal must induce the progenitor cells to
produce either neuroblasts or glioblasts. Finally, a chemical signal, or perhaps even a
set of signals, must induce the genes to make a particular type of neuron.
One class of compounds that signal cells to develop in particular ways are called
neurotrophic factors. By removing stem cells from the brain of an animal and placing
those cells in solutions that keep them alive, researchers can study how neurotrophic
factors function. When one compound, known as epidermal growth factor (EGF), is
added to the cell culture, it stimulates stem cells to produce progenitor cells. Another
compound, basic fibroblast growth factor (bFGF), stimulates progenitor cells to produce
neuroblasts.
At this point, the destiny of a given neuroblast is not predetermined. The blast can
become any type of neuron if it receives the right chemical signal. The body relies on a
“general-purpose neuron” that, when exposed to certain neurotrophic factors,matures
into the specific type of cell that the nervous system requires in a particular location.
This flexibility makes brain development simpler than it would be if each different
type of cell, as well as the number of cells of each type, had to be precisely specified
in an organism’s genes. In the same way, building a house from “all purpose”
two-by-fours that can be cut to any length as needed is easier than specifying in a blueprint
a precise number of precut pieces of lumber that can be used only in a certain
location.
Growth and Development of Neurons
In human brains, approximately 10 billion (1010) cells are needed to form just the cortex
that blankets a single hemisphere. To produce such a large number of cells, about
250,000 neurons must be born per minute at the peak of prenatal brain development.
But, as Table 6-1 shows, this rapid formation of neurons and glia is just the first step
in the growth of a brain. These cells must travel to their correct locations (a
process called migration), they must differentiate into the right type of neuron
or glial cell (see Figure 6-10), and the neurons must grow dendrites and
axons and subsequently form synapses.
Recall that the brain must also prune back unnecessary cells and connections,
sculpting itself according to the experiences and needs of the particular
person.We consider each of these stages in brain development next, focusing
on the development of the cerebral cortex, because more is known about cortical
development than about the development of any other area of the human
brain. However, the principles derived from our examination of the cortex
apply to neural growth and development in other brain regions as well.
NEURAL GENERATION,MIGRATION,
AND DIFFERENTIATION
In humans, as in other vertebrates, the brain begins as part of the neural tube, the part
that contains the cells from which the brain will form. Figure 6-11 shows that the generation
of the cells that will eventually form the cortex begins about 7 weeks after conception
and is largely complete by 20 weeks. In other words, neurogenesis (the process
of forming neurons) is largely finished after about 5 months of gestation, approximately
the time at which prematurely born infants have some chance of surviving.
During the next 5 months, until just after full-term birth, the fetal brain is especially
delicate and extremely vulnerable to injury, teratogens (chemicals that cause malformations),
and trauma, including anoxia, as explained in “Cerebral Palsy” on page 196.
Neurotrophic factor. A chemical
compound that acts to support growth
and differentiation in developing neurons
and may act to keep certain neurons alive
in adulthood.
Stages of Brain Development
1. Cell birth (neurogenesis; gliogenesis)
2. Cell migration
3. Cell differentiation
4. Cell maturation (dendrite and axon growth)
5. Synaptogenesis (formation of synapses)
6. Cell death and synaptic pruning
7. Myelogenesis (formation of myelin)
Table 6-1
For more information on development
of the brain and nervous system, as well
as their effect on behavior, visit the
Chapter 6 Web links on the Brain and
Behavior Web site (www.worth
publishers.com/kolb).
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196 ! CHAPTER 6
200
2000
500
1000
4000
3000
400
300
20
50
100
40
30
10
Conception Age (in weeks)
Brain weight
Body weight
9 18 27
Relative size (in grams)
36 38 Birth 40
Neuronal migration Differentiation Neuronal maturation
Neurogenesis
Figure 6-11
Development of the Human Cerebral
Cortex The cortex begins to form
about 6 weeks after conception, with
neurogenesis largely complete by
20 weeks. Neural migration and cell
differentiation begin at about 8 weeks
and are largely complete by about
29 weeks. Neuron maturation, including
axon and dendrite growth, begins at
about 20 weeks and continues until well
after birth. Both brain weight and body
weight increase rapidly and in parallel
during the prenatal period. Adapted from
“Pathogenesis of Late-Acquired Leptomeningeal
Heterotopias and Secondary Cortical Alterations:
A Golgi Study,” by M. Marin-Padilla, in Dyslexia
and Development: Neurobiological Aspects of
Extraordinary Brains (p. 66), edited by A. M.
Galaburda, 1993, Cambridge, MA: Harvard
University Press.
Cerebral Palsy
Focus on Disorders
We met Patsy when she took our introductory course on
brain and behavior. She walked with a peculiar shuffle; her
handwriting was almost illegible; and her speech was at
times almost unintelligible. Patsy had cerebral palsy, and she
earned an A in the course.
William Little, an English physician, first noticed in 1853
that difficult or abnormal births could lead to later motor difficulties
in children. The disorder that Little described was
cerebral palsy, although it has also been called Little’s disease.
Cerebral palsy is common worldwide, with an incidence
estimated to be 1.5 in every 1000 births. Among
surviving babies who weigh less than 2.5 kilograms at birth,
the incidence is much higher—about 10 in every 1000.
The most common cause of cerebral palsy is birth injury,
especially due to anoxia, a lack of oxygen. Anoxia
may result from a defect in the placenta, the organ that allows
oxygen and nutrients to pass from mother to child, or
it may be caused by an entanglement of the umbilical cord
during birth, which may reduce the oxygen supply to the
infant. Other causes include infections, hydrocephalus,
seizures, and prematurity. All produce a defect in the immature
brain, either before, during, or just after birth.
Most children with cerebral palsy appear normal in the
first few months of life but, as the nervous system develops,
the motor disturbances become progressively more noticeable.
The most common symptom, which afflicts about half
of those affected, is spasticity, or exaggerated contraction of
muscles when they are stretched. Not surprisingly, spasticity
often interferes with other motor functions. For example,
people with cerebral palsy may have an odd gait, sometimes
dragging one foot.
A second common symptom is dyskinesia, involuntary
extraneous movements such as tremors and uncontrollable
jerky twists, called athetoid movements, which
often occur in activities such as walking. A third common
symptom is rigidity, or resistance to passive movement.
For example, a patient’s fingers may resist being moved
passively by an examiner, even though the patient is able
to move the fingers voluntarily. In addition to having these
motor symptoms, people with cerebral palsy are at risk for
retardation, although many, Patsy included, function at a
high intellectual level and earn college and postgraduate
degrees.
Apparently, the developing brain can more easily cope with injury earlier, during the
time of neuron generation, than it can during the final stages of cell migration or cell
differentiation, which is the first stage in cell maturation. One reason may be that,
once neurogenesis has stopped, it is very hard to start it again. If neurogenesis is still
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progressing, it may be possible to make more neurons to replace injured ones or perhaps
existing neurons can be allocated differently.
The same is true in supplying the lumber for a house. If some of the lumber is
damaged in milling, the damaged pieces can be replaced easily. But, if the lumber is
damaged in transit or on site, it is not so easy to replace, especially if the mill is closed.
Replacement is even more difficult if the lumber has already been cut to size for a specific
use.
Cell migration begins shortly after the first neurons are generated, but it continues
for about 6 weeks after neurogenesis is complete. At this point, the process of cell
differentiation, in which neuroblasts become specific types of neurons, begins. Cell differentiation
is essentially complete at birth, although neuron maturation, which includes
the growth of dendrites, axons, and synapses, goes on for years and, in some
parts of the brain, may continue throughout adulthood.
As you learned in Chapter 2, the cortex is organized into layers that are distinctly
different from one another in their cellular makeup. How is this arrangement of differentiated
areas created during development? Pasko Rakic and his colleagues have
been finding answers to this question for more than three decades.Apparently, the ventricular
zone contains a primitive map of the cortex that predisposes cells formed in a
certain ventricular region to migrate to a certain cortical location. For example, one region
of the ventricular zone may produce cells destined to migrate to the visual cortex,
whereas another region produces cells destined to migrate to the frontal lobes.
But how do the cells know where these different parts of the cortex are located?
They follow a path made by radial glial cells. Each of these path-making cells has a
fiber that extends from the ventricular zone to the surface of the cortex, as illustrated
in Figure 6-12A. The close-up view in Figure 6-12B shows that neural cells from a given
region of the ventricular zone need only follow the glial road and they will end up in
the right location.
The advantage of this system is that, as the brain grows, the glial fibers stretch
but they still go to the same place. Figure 6-12A also shows a non-radially migrating
cell that is moving perpendicularly to the radial glial fibers. Although most cortical
neurons follow the radial glial fibers, a small number appear to migrate by seeking
some type of chemical signal. Researchers do not yet know why these cells function
differently.
Cortical layers develop from the inside out,much like adding layers to a tennis ball.
The neurons of innermost layer VI migrate to their locations first, followed by those
destined for layer V, and so on, as successive waves of neurons pass
earlier-arriving neurons to assume progressively more exterior positions
in the cortex. The formation of the cortex is a bit like building
a house from the ground up until you reach the roof. The materials
needed to build higher floors must pass through lower floors to get
to their destinations.
One thing that facilitates the building of a house is that each new
story has a blueprint-specified dimension, such as 8 feet high. How
do neurons determine how thick a cortical layer should be? This is a
tough question, especially when you consider that the layers of the
cortex are not all the same thickness.
Probably the answer is partly related to timing. Cells destined for
a certain layer are generated at a certain time in the ventricular zone,
and so they migrate together in that particular time frame. The
mechanisms that govern this timing are not yet understood, however.
In addition, some local environmental signals—chemicals produced
by other cells—likely influence the way in which cells form layers
in the cortex. These intercellular signals progressively restrict the
HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 197
Primitive
cortex
Ventricular
zone
(A) (B)
Brain surface
Direction of
movement
Radial glial process
Migrating
neuron
Radial glial
cell body
Migrating neuron
Radial glial
processes
Non-radially
migrating neuron
Figure 6-12
Neural Migration Neuroscientists
hypothesize that the map for the cortex
is represented in the ventricular zone.
(A) Radial glial fibers extend from the
ventricular zone to the cortical surface.
(B) Neurons migrate along the radial
glial fibers, which take them from the
protomap in the ventricular zone to the
respective region in the cortex. Adapted
from “Neurons in Rhesus Monkey Cerebral Cortex:
Systematic Relation Between Time of Origin and
Eventual Disposition,” by P. Rakic, 1974, Science,
183, p. 425.
Radial glial cell. Path-making cell that a
migrating neuron follows to its
appropriate destination.
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choice of traits that a cell can express, as illustrated in Figure 6-13.
Thus, the emergence of distinct types of cells in the brain does not
result from the unfolding of a specific genetic program. Instead, it is
due to the interaction of genetic instructions, timing, and signals
from other cells in the local environment.
NEURAL MATURATION
After neurons migrate to their final destinations and differentiate
into specific neuron types, they begin to mature in two ways.Maturing
neurons grow dendrites to provide the surface area for synapses
with other cells, and they extend their axons to appropriate targets to
initiate synapse formation.
Two events take place in the development of a dendrite: dendritic arborization
(branching) and the growth of dendritic spines.As illustrated in Figure 6-14, dendrites
begin as individual processes protruding from the cell body. Later, they develop increasingly
complex extensions that look much like the branches of trees visible in winter;
that is, they undergo arborization. The dendritic branches then begin to form
spines, which are the location of most synapses on the dendrites.
Although dendritic development begins prenatally in humans, it continues for a long
time after birth, as Figure 6-14 shows. Dendritic growth proceeds at a slow rate, on the
order of micrometers per day. Contrast this rate with that of the development of axons,
which grow on the order of a millimeter per day, about a thousand times as fast. The disparate
developmental rates of axons and dendrites are important because the faster-growing
axon can contact its target cell before the dendrites of that cell are completely formed.
In this way, the axon may play a role in dendritic differentiation and, ultimately, in neuron
function—for example, as part of the visual,motor, or language circuitry of the brain.
Axon-appropriate connections may be millimeters or even centimeters away in the
developing brain, and the axon must find its way through a complex cellular terrain to
make them. Axon connections present a significant engineering problem for the developing
brain. Such a task could not possibly be specified in a rigid genetic program.Rather,
genetic–environmental interaction is at work again as the formation of axonic connections
is guided by various molecules that attract or repel the approaching axon tip.
Santiago Ramón y Cajal was the first to describe this developmental process a century
ago. He called the growing tips of axons growth cones. Figure 6-15A shows that,
198 ! CHAPTER 6
Uncommitted
precursor
Cells with
some segregation
of determinants
Further
segregation
of determinants
Intercellular
environment
Diverse
cells
Figure 6-13
Cellular Commitment As diagrammed
in Figure 6-10, precursor cells have an
unlimited cell-fate potential but, as they
develop, the interaction of genes,
maturation, and environmental
influences increasingly steer them
toward a particular cell type.
Newborn 1 3 6
Age (months)
15 24
Figure 6-14
Neural Maturation In postnatal
differentiation of the human cerebral
cortex—shown here around Broca’s area,
which controls speaking—the neurons
begin with simple dendritic fields that
become progressively more complex
until a child reaches about 2 years of
age. Thus brain maturation parallels the
development of a behavior—that is, the
emergence of language. Adapted from
Biological Foundations of Language (pp. 160–
161), by E. Lenneberg, 1967, New York: Wiley.
You can use your Foundations of
Behavioral Neuroscience CD to review
the structure of dendrites. Visit the
module on neural communication and
look at the overview of a neuron’s
structure. (See the Preface for more
information about this CD.)
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as these growth cones extend, they send out shoots, analogously to fingers reaching out
to find a pen on a cluttered desk.When one shoot, known as a filopod (plural, filopodia),
reaches an appropriate target, the others follow. Figure 6-15B charts the growth
of a hypothetical axon tip and its growth-cone extensions over time.
Growth cones are responsive to two types of cues:
1. Cell-adhesion molecules (CAMs) are cell-manufactured molecules that either lie
on the cell surface or are secreted into the intercellular space. Some CAMs provide
a surface to which growth cones can adhere, hence their name, whereas others
serve to attract or repel growth cones.
2. Tropic molecules, to which growth cones respond, are produced by the targets being
sought by the axons. (Tropic molecules, which guide axons, should not be confused
with the trophicmolecules,discussed earlier, that support the growth of neurons and
their processes.) Tropic molecules essentially tell growth cones to “come over here.”
They likely also tell other growth cones seeking different targets to “keep away.”
Although Ramón y Cajal predicted tropic molecules more than 100 years ago, they
have proved difficult to find. Only one group, netrins (from Sanskrit for “to guide”),
has been identified so far.Given the enormous number of connections in the brain and
the great complexity in wiring them,many other types of tropic molecules are likely to
be found.
SYNAPTIC DEVELOPMENT
The number of synapses in the human cerebral cortex is staggering, on the order of
1014. This huge number could not possibly be determined by a genetic program that
assigns each synapse a specific location. Instead, only the general outlines of neural
connections in the brain are likely to be genetically predetermined. The vast array of
specific synaptic contacts is then guided into place by a variety of environmental cues
and signals.
A human fetus displays simple synaptic contacts in the fifth gestational month. By
the seventh gestational month, synaptic development on the deepest cortical neurons
is extensive. After birth, the number of synapses increases rapidly. In the visual cortex,
synaptic density almost doubles between age 2 months and age 4 months and then continues
to increase until age 1 year.
CELL DEATH AND SYNAPTIC PRUNING
If you wanted to make a statue, you could start either with grains of sand and glue them
together to form the desired shape or with a block of stone and chisel the unwanted
pieces away. Sculptors consider the second route much easier. They start with more
than they need and eliminate the excess. So does the brain, and it is the value of cell
HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 199
Growth cone. Growing tip of an axon.
Filopod. Process at the end of a
developing axon that reaches out to
search for a potential target or to sample
the intercellular environment.
Cell-adhesion molecule (CAM). A
chemical to which specific cells can
adhere, thus aiding in migration.
Tropic molecule. Signaling molecule
that attracts or repels growth cones.
Netrins. The only class of tropic
molecules yet isolated.
(A) (B)
0.1
0
Time (minutes)
Size (mm)
0 9 14 23 31 38
Growth cone
Filopodia
Figure 6-15
Seeking a Path (A) At the tip of this
axon, nurtured in a culture, a growth
cone sends out filopodia seeking specific
molecules to guide the axon’s growth
direction. (B) Growth in the axon tip and
its growth cones over time.
Courtesty of Dennis Bray
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death and synaptic pruning. The “chisel” in the brain could be of
several forms, including a genetic signal, experience, reproductive
hormones, and even stress.
For example, as already stated, the number of synapses in the
visual cortex increases rapidly after birth, reaches a peak at about
1 year, and begins to decline as the brain apparently prunes out unnecessary
or incorrect synapses. The graph in Figure 6-16 plots
this rise and fall in synaptic density. Pasko Rakic estimated that, at
the peak of synapse loss in humans, as many as 100,000 synapses
may be lost per second.We can only wonder what the behavioral
consequence of this rapid synaptic loss might be. It is probably no
coincidence that children, especially toddlers and adolescents,
seem to change moods and behaviors quickly.
How does the brain accomplish this elimination of neurons?
The simplest explanation is competition, sometimes referred to as
neural Darwinism. Charles Darwin believed that one key to evolution
is the production of variation in the traits that a species
possesses. Certain traits can then be selected by the environment for their favorableness
in aiding survival. According to a Darwinian perspective, then, more animals are
born than can survive to adulthood, and environmental pressures “weed out” the lessfit
ones. Similar pressures cause neural Darwinism.
What exactly is causing this weeding out of cells in the brain? It turns out that,
when neurons form synapses, they become somewhat dependent on their targets for
survival. In fact, deprived of synaptic targets, they eventually die. This neuron death
occurs because target cells produce neurotrophic factors, which we encountered earlier,
that are absorbed by the axon terminals and function to regulate neuronal survival.
Nerve growth factor (NGF), for example, is made by cortical cells and absorbed by
cholinergic neurons in the basal forebrain.
If many neurons are competing for a limited amount of a neurotrophic factor, only
some of those neurons can survive. The death of neurons deprived of a neurotrophic
factor is different from the cell death caused by injury or disease. When neurons are
deprived of a neurotrophic factor, certain genes seem to be “turned on,” resulting in a
message for the cell to die. This programmed process is called apoptosis.
Apoptosis accounts for the death of overabundant neurons, but it does not account
for the pruning of synapses from cells that survive. In 1976, French neurobiologist
Jean-Pierre Changeux proposed a theory for synapse loss that also is based on competition.
According to Changeux, synapses persist into adulthood only if they have become
members of functional neural networks. If they have not, they are eventually
eliminated from the brain.
An example will help explain this mechanism of synaptic pruning. Consider neural
input to the midbrain from the eyes and ears. The visual input goes to the superior
colliculus, and the auditory input goes to the inferior colliculus (see Figure 2-18). Some
errant axons from the auditory system will likely end up in the visual midbrain and
form synapses with the same cells as those connected to axons coming from the visual
pathway.
However, the auditory axons are not part of functional networks in this location.
Whereas inputs from an eye are apt to be active at the same time as one another, inputs
from an ear are unlikely to be active along with the visual ones. The presence of
simultaneous electrical activity in a set of visually related synapses leads to the formation
of a neural circuit comprising those synapses.
In contrast, the errant auditory inputs, because they are not active at the same time
as the visual inputs, become unstable and are eventually eliminated.We can speculate
200 ! CHAPTER 6
Neural Darwinism. Hypothesis that the
processes of cell death and synaptic
pruning are, like natural selection in
species, the outcome of competition
among neurons for connections and
metabolic resources in a neural
environment.
Apoptosis. Cell death that is genetically
programmed.
Number of synapses (!1011)
7
months
gestation
Birth
2 4 6 8 1012 2 5 10 20 30 50 70
8
4
12
16
20
24
0
Months
Year Prenatal 1 Subsequent years
Years
Figure 6-16
Synaptic Pruning An estimate of the
synapses in the human visual cortex as a
function of age shows that the total
rises rapidly, peaking at about 1 year;
declines until about 10 years of age;
and levels off until early adulthood,
when it gradually begins to drop again
over the remaining life span. Adapted from
“Synaptogenesis in Human Cerebral Cortex,” by
P. R. Huttenlocher, in Human Behavior and the
Developing Brain (p. 142), edited by G. Dawson
and K. W. Fischer, 1994, New York: Guilford Press.
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that environmental factors such as hormones, drugs, and experience would influence
the formation of active neural circuits and thus influence the processes of synapse stabilization
and pruning. In fact, as you will see shortly, experience can have truly massive
effects on the organization of the nervous system.
In addition to outright errors in synapse formation
that give rise to synaptic pruning, more-subtle changes
in neural circuits may trigger the same process. An instance
of such a change accounts for the findings of
Janet Werker and Richard Tees (1992), who studied the
ability of infants to discriminate speech sounds taken
from widely disparate languages, such as English,Hindi
(from India), and Salish (a Native American language).
Their results show that young infants can discriminate speech sounds of different languages
without previous experience, but their ability to do so declines in the first year of
life.One explanation of this declining ability is that synapses encoding speech sounds not
normally encountered in the infant’s daily environment are not active simultaneously
with other speech-related synapses.As a result, they become unstable and are eliminated.
Synapse elimination is extensive. Peter Huttenlocher (1994) estimated it to be 42
percent of all synapses in the human cortex. Synapse elimination is much less extensive
in smaller-brained animals, however. In the rat cortex, it is about 10 percent, and,
in the cat cortex, about 30 percent. The reason for these differences may be that, the
larger the brain, the more difficult it is to make precise connections and so the greater
the need for excess synapses and the consequent synaptic pruning.
Synaptic pruning may also allow the brain to adapt more flexibly to environmental
demands. Human cultures are probably the most diverse and complex environments
with which any animal must cope. Perhaps the flexibility in cortical organization
that is achieved by the mechanism of selective synaptic pruning is a necessary precondition
for successful development in this kind of environment.
Synaptic pruning may also be a precursor related to different perceptions that people
develop about the world. Consider, for example, the obvious differences in “Eastern”
and “Western” philosophies about life, religion, and culture. Given the obvious
differences to which the brains of people in the East and West are exposed as their
brains develop, we can only imagine how differently their individual perceptions and
cognitions may be. Considered together as a species, however, we humans are far more
alike than we are different.
Glial Development
The birth of astrocytes and oligodendrocytes begins after most neurogenesis is complete
and continues throughout life. As you know from Chapter 3, oligodendroglia
form the myelin that surrounds axons in the spinal cord and brain. Although CNS
axons can function before they are myelinated, normal adult function is attained only
after myelination is complete. Consequently, myelination is a useful rough index of
cerebral maturation.
In the early 1920s, Paul Flechsig noticed that myelination of the cortex begins just
after birth and continues until at least 18 years of age. He also noticed that some cortical
regions were myelinated by age 3 to 4 years, whereas others showed virtually no
myelination at that time. Figure 6-17 shows one of Flechsig’s cortical maps with areas
shaded according to earlier or later myelination. Flechsig hypothesized that the earliestmaturing
areas control simple movements or sensory analyses, whereas the latestmyelinating
areas control the highest mental functions.
HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 201
Richard Tees Janet Werker
Figure 6-17
Progress of Myelination In this
cortical map, based on Flechsig’s
research, the light-colored zones are
very late to myelinate, which led Flechsig
to propose that their functions are
qualitatively different—that is, more
complex—from those that mature
earlier.
On your Foundations CD, you can
review the myelination of axons and how
it affects neural transmission. To view an
animation of this process, go to the area
on the conduction of the action potential
in the module on neural communication.
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CORRELATING BEHAVIOR WITH BRAIN DEVELOPMENT
It is reasonable to predict that, as a particular brain area matures, a person exhibits behaviors
corresponding to that particular mature brain structure. The strongest advocate
of this view has been Eric Lenneberg,who, in 1967, published a seminal book titled
Biological Foundations of Language. A principal theme is that children’s acquisition of
language is tied to the development of critical language areas in the cerebral cortex.
This idea immediately stimulated debate about the merits of correlating brain and
behavioral development. Now, some 40 years later, the relation is widely accepted, although
the influence of environmental factors such as experience and learning on behavior
is still considered critical. That is, psychologists believe that behaviors cannot
emerge until the neural machinery for them has developed, but, when that machinery
is in place, related behaviors develop quickly through stages and are shaped significantly
by experience. The new behaviors then alter brain structure by the processes of
neural Darwinism presented earlier.
Researchers have studied these interacting changes in the brain and behavior, especially
in regard to the emergence of motor skills, language, and problem solving in
children.We now explore each of these developments.
Motor Behaviors
The development of locomotion skills is easy to observe in human infants. At first,
babies are unable to move about independently but, eventually, they learn to crawl
and then to walk.Other motor skills develop in less obvious but no less systematic ways.
For example, Tom Twitchell (1965) studied and described how the ability to reach for
objects and grasp them progresses in a series of stages, illustrated in Figure 6-18.
Shortly after birth, infants are capable of flexing the joints of an arm in such a way
that they can scoop something toward their bodies, but, newborns do not seem to direct
their arm movements toward any specific thing. Then, between
1 and 3 months of age, a baby begins to orient a hand
toward an object that the hand has touched and gropes to
hold that object. For example, if the baby’s hand touches a
stick, the fingers will flex to grasp it.At this stage, however, all
the fingers flex together.At this time babies also begin to make
spontaneous hand and digit movements, a kind of “motor
babbling” (Wallace & Whishaw, 2003).
Between 8 and 11 months, infants’ grasping becomes
more sophisticated as the “pincer grasp,” employing the index
In Review .
The first neural stem cell heralds brain development in the 3-week-old human embryo. Beginning
as a sheet of cells that folds to become the neural tube, nervous system formation then
proceeds rapidly; by about 100 days after conception, the brain begins to take a recognizably
human form. Neurons and glia develop through a series of seven stages: birth, migration, differentiation,
maturation, synaptic formation, cell death, and myelination. Neurons begin to
process simple information before they are completely mature, but behavioral development
is constrained by the maturation of central nervous system structures and circuits. For example,
although infants and children are capable of complex movements, not until myelination
is complete in adolescence are adult levels of coordination and fine motor control reached.
202 ! CHAPTER 6
Figure 6-18
Development of the Grasping
Response of Infants Adapted from “The
Automatic Grasping Response of Infants,” by
T. E. Twitchell, 1965, Neuropsychologia, 3, p. 251.
2 months 4 months 10 months
Orients hand toward
an object and gropes
to hold it.
Grasps appropriately
shaped object with
entire hand.
Uses pincer grasp with
thumb and index
finger opposed.
CH06.qxd 1/28/05 10:14 AM Page 202

finger and the thumb, develops. The pincer grasp is a significant development because it
allows babies to make the very precise finger movements needed to manipulate small objects.
What we see, then, is a sequence in the development of grasping: first scooping, then
grasping with all the fingers, and then grasping by using independent finger movements.
If the development of increasingly well coordinated grasping depends on the
emergence of certain neural machinery, anatomical changes in the brain should accompany
the emergence of these motor behaviors. Probably many such changes take
place, especially in the development of dendritic arborizations. And a correlation between
myelin formation and the ability to grasp has been found (Yakovlev & Lecours,
1967). In particular, a group of axons from motor-cortex neurons become myelinated
at about the same time that reaching and grasping with the whole hand develop. Another
group of motor-cortex neurons, which are known to control finger movements,
become myelinated at about the time that the pincer grasp develops.
We can now make a simple prediction. If specific motor-cortex neurons are essential
for adultlike grasping movements to emerge, the removal of those neurons should
make an adult’s grasping ability similar to that of a young infant, which is in fact what
happens.One of the classic symptoms of damage to the motor cortex is the permanent
loss of the pincer grasp, as you will learn in Chapter 10.
Language Development
The acquisition of speech follows a gradual series of developments that has usually progressed
quite far by the age of 3 or 4.According to Lenneberg, children reach certain important
speech milestones in a fixed sequence and at constant chronological ages. These
milestones are summarized in Table 6-2.
Although language skills and motor skills generally develop in parallel, the capacity
for language depends on more than just the ability to make controlled movements of
the mouth, lips, and tongue. Precise movements of the muscles controlling these body
parts develop well before children can speak. Furthermore, even when children have sufficient
motor skill to articulate most words, their vocabularies do not rocket ahead but
rather progress gradually.
A small proportion of children (about 1 percent) have normal intelligence and normal
motor-skill development, and yet their speech acquisition is markedly delayed. Such
children may not begin to speak in phrases until after age 4,despite an apparently normal
environment and the absence of any obvious neurological signs of brain damage. Because
the timing of the onset of speech appears universal in the remaining 99 percent of
children across all cultures, something different is likely to occur in the brain maturation
of a child with late language acquisition. But it is hard to specify what that difference is.
Because the age of language onset is usually between 1 and 2 and language acquisition
is largely complete by age 12, the best strategy is to consider how the cortex is
different before and after these two milestones. By age 2, cell division and migration
are complete in the language zones of the cerebral cortex. The major changes that take
place between the ages of 2 and 12 are in the interconnections of neurons and the
myelination of the speech zones.
The changes in dendritic complexity in these areas are among the most impressive in
the brain. Recall from Figure 6-14 that the axons and dendrites of the speech zone called
Broca’s area are simple at birth but grow dramatically more dense between 15 and 24
months of age. This neural development correlates with an equally dramatic change in
language ability, given that a baby’s vocabulary starts to expand rapidly at about age 2 (see
Table 6-2).
We can therefore infer that language development may be constrained, at least in
part, by the maturation of language areas in the cortex. Individual differences in the
HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 203
Visit the Chapter 6 Web links on the
Brain and Behavior Web site to see other
examples of motor development in
childhood.
CH06.qxd 1/28/05 10:14 AM Page 203

speed of language acquisition may be accounted for by differences in this neural development.
Children with early language abilities may have early maturation of the
speech zones, whereas children with delayed language onset may have later speechzone
maturation.
Development of Problem-Solving Ability
The first person to try to identify discrete stages of cognitive development was Swiss
psychologist Jean Piaget (1952). He realized that he could infer children’s understanding
of the world by observing their behavior. For example, a baby who lifts a cloth to
retrieve a hidden toy is showing an understanding that objects continue to exist even
when out of sight. This understanding, the concept of object permanence, is revealed by
the behavior of the infant in the upper photographs of Figure 6-19.
An absence of understanding also can be seen in children’s behavior, as shown by
the actions of the 5-year-old girl in the lower photographs of Figure 6-19. She was
shown two identical beakers with identical volumes of liquid in each and then watched
204 ! CHAPTER 6
Developmental Milestones for Basic Language Functions
Approximate age Basic social and language functions
Birth Comforted by sound of human voice; most common utterances are
discomfort and hunger cries
6 weeks Responds to human voice and makes cooing and pleasure noises; cries
to gain assistance
2 months Begins to distinguish different speech sounds; cooing becomes more
guttural, or “throaty”
3 months Orients head to voices; makes a vocal response to others’ speech; begins
babbling, or chanting various syllabic sounds in a rhythmic fashion
4 months Begins to vary pitch of vocalizations; imitates tones
6 months Begins to imitate sounds made by others
9 months Begins to convey meaning through intonation, using patterns that
resemble adult intonations
12 months Starts to develop a vocabulary; a 12-month-old may have a vocabulary
of 5 to 10 words that will double in the next 6 months
24 months Vocabulary expands rapidly and can consist of approximately 200 to 300
words; names most common everyday objects; most utterances are
single words
36 months Has vocabulary of 900 to 1000 words; 3- to 4-word simply constructed
sentences (subject and verb); can follow two-step commands
4 years Has a vocabulary of more than 1500 words; asks numerous questions;
sentences become more complex
5 years Typically has a vocabulary of approximately 1500 to 2200 words;
discusses feelings; the average 5- to 7-year-old has acquired a slow but
fluent ability to read; handwriting likely to be slow
6 years Speaks with a vocabulary of about 2600 words; understands from
20,000 to 24,000 words; uses all parts of speech
Adult Has 50,000" word vocabulary by 12 years old
Adapted from “Development of the Child’s Brain and Behavior,” by B. Kolb and B. Fantie, in Handbook of
Clinical Child Neuropsychology (2nd ed., p. 29), edited by C. R. Reynolds and E. Fletcher-Janzen, 1997, New York:
Plenum.
Table 6-2
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HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 205
as one beaker’s liquid was poured into a taller, narrower beaker. When asked which
beaker contained more liquid, she pointed to the taller beaker, not understanding that
the amount of liquid remains constant despite the difference in appearance. Children
display an understanding of this principle, the conservation of liquid volume, at about
age 7.
By studying children engaged in such tasks, Piaget concluded that cognitive development
is a continuous process. Children’s strategies for exploring the world and their
understanding of it are constantly changing. These changes are not simply the result of
acquiring specific pieces of new knowledge. Rather, at certain points in development,
fundamental changes take place in the organization of a child’s strategies for learning
about the world and for solving problems.With these developing strategies comes new
understanding.
Piaget identified four major stages of cognitive development, which are summarized
in Table 6-3:
Stage I is the sensorimotor period, from birth to about 18 to 24 months of age.During
this time, babies learn to differentiate themselves from the external world, come to
realize that objects exist even when out of sight, and gain some understanding of causeand-
effect relations.
Stage II, the preoperational period, extends from ages 2 to 6 years. Children gain the
ability to form mental representations of things in their world and to represent those
things in words and drawings.
Stage III is the period of concrete operations, typically from ages 7 to 11 years. Children
are able to mentally manipulate ideas about material (concrete) things such as
volumes of liquid, dimensions of objects, and arithmetic problems.
Stage IV, the period of formal operations, is attained sometime after age 11.
Children are now able to reason in the abstract, not just in concrete terms.
If we take Piaget’s stages as rough approximations of qualitative changes that take
place in children’s thinking as they grow older, we can ask what neural changes might
Figure 6-19
Stages of Cognitive Development
(Top) The infant shows that she
understands object permanence—that
things continue to exist when they are
out of sight. (Bottom) This girl does not
yet understand the principle of
conservation of volume. Beakers with
identical volumes but different shapes
seem to her to hold different amounts
of liquid.
Courtesy of Don and Sandy Hockenbury Doug Goodman/Monkmeyer
Visit the Chapter 6 Web links on the
Brain and Behavior Web site
(www.worthpublishers.com/kolb)
for more information on Piaget’s stages of
cognitive development.
CH06.qxd 1/28/05 10:14 AM Page 205

underlie them.One place to look for brain changes
is in the relative rate of brain growth.
After birth, brain and body do not grow uniformly
but rather tend to increase in mass during
irregularly occurring periods commonly called
growth spurts. In his analysis of brain-weightto-
body-weight ratios, Herman Epstein (1979)
found consistent spurts in brain growth between
3 and 10 months (accounting for an increase of
30 percent in brain weight by the age of 11/2 years)
as well as from the ages of 2 to 4, 6 to 8, 10 to 12,
and 14 to 16" years. The increments in brain
weight were from about 5 to 10 percent in each
of these 2-year periods.
Brain growth takes place without a concurrent
increase in the number of neurons, and so it
is most likely due to the growth of glial cells and
synapses. Although synapses themselves would
be unlikely to add much weight to the brain, the
growth of synapses is accompanied by increased
metabolic demands, which cause neurons to become
larger, new blood vessels to form, and new
astrocytes to be produced.
We would expect such an increase in the complexity of the cortex to generate
more-complex behaviors, and so we might predict significant, perhaps qualitative,
changes in cognitive function during each growth spurt. The first four brain-growth
spurts identified by Epstein coincide nicely with the four main stages of cognitive development
described by Piaget. Such correspondence suggests significant alterations in
neural functioning with the onset of each cognitive stage.
At the same time, differences in the rate of brain development or perhaps in the
rate at which specific groups of neurons mature may account for individual differences
in the age at which the various cognitive advances identified by Piaget emerge. Although
Piaget did not identify a fifth stage of cognitive development in later adolescence,
the presence of a growth spurt then implies one.
One difficulty in linking brain-growth spurts to cognitive development is that
growth spurts are superficial measures of changes taking place in the brain. We need
to know at a deeper level what neural events are contributing to brain growth and just
where they are taking place.
A way to find out is to observe children’s attempts to solve specific problems that
are diagnostic of damage to discrete brain regions in adults. If children perform a particular
task poorly, then whatever brain region regulates the performance of that task
in adults must not yet be mature in children. Similarly, if children can perform one task
but not another, the tasks apparently require different brain structures, and these structures
mature at different rates.
Bill Overman and Jocelyn Bachevalier (Overman, Bachevalier, Turner, & Peuster,
1992) used this logic to study the development of forebrain structures required for
learning and memory in young children and in monkeys. The Procedure
section of Experiment 6-1 shows the three intelligence-test
items presented to their subjects. The first task was simply to learn
to displace an object to obtain a food reward.When the subjects had
learned this displacement task, they were trained in two more tasks
believed to measure the functioning of the temporal lobes and the
basal ganglia, respectively.
206 ! CHAPTER 6
Growth spurt. Sproradic period of
sudden growth that lasts for a finite time. Bill Overman
Piaget’s Stages of Cognitive Development
Developmental
Typical age range Description of stage phenomena
Object permanence
Stranger anxiety
Pretend play
Egocentrism
Language
development
Conservation
Mathematical
transformations
Abstract logic
Potential for mature
moral reasoning
Stage I: Sensorimotor
Experiences the world through
senses and actions (looking,
touching, mouthing)
Stage II: Preoperational
Represents things with words
and images but lacks logical
reasoning
Stage III: Concrete operational
Thinks logically about concrete
events; grasps concrete
analogies and performs
arithmetical operations
Stage IV: Formal operational
Reasons abstractly
Birth to 18–
24 months
About 2–6 years
About 7–11 years
About 12" years
Table 6-3
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HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 207
In the nonmatching-to-sample task, the subjects
were shown an object that they could displace to receive
a food reward. After a brief (15-second) delay,
two objects were presented: the first object and a novel
object. The subjects then had to displace the novel object
to obtain the food reward. Nonmatching to sample
is thought to measure object recognition, which is
a function of the temporal lobes. The subject can find
the food only by recognizing the original object and
not choosing it.
In the third task, concurrent discrimination, the
subjects were presented with a pair of objects and had
to learn that one object in that pair was always associated
with a food reward, whereas the other object was
never rewarded. The task was made more difficult by
sequentially giving the subjects 20 different object
pairs. Each day, they were presented with one trial per
pair. Concurrent discrimination is thought to measure
trial-and-error learning of specific object information,
which is a function of the basal ganglia.
Adults easily solve both the nonmatching and the
concurrent tasks but report that the concurrent task is
more difficult because it requires remembering far
more information. The key question developmentally
is whether there is a difference in the age at which children
(or monkeys) can solve these two tasks.
It turns out that children can solve the concurrent
task by about 12 months of age, but not until
about 18 months of age can they solve what most
adults believe to be the easier nonmatching task.
These results imply that the basal ganglia, the critical
area for the concurrent-discrimination task, mature
more quickly than the temporal lobe, which is the
critical region for the nonmatching-to-sample task.
A Caution about Linking
Correlation to Causation
Throughout this section, we have described research
that implies that changes in the brain cause changes
in behavior. Neuroscientists assert that, by looking at
behavioral development and brain development in
parallel, they can make some inferences regarding the
causes of behavior. Bear in mind, however, that just
because two things correlate (take place together)
does not prove that one of them causes the other.
The correlation–causation problem raises red
flags in studies of brain and behavior, because research
in behavioral neuroscience, by its very nature,
is often based on such correlations. Nevertheless, correlational studies, especially developmental
correlational studies, have proved to be a powerful tool as sources of insight
into fundamental princples of brain and behavior.
– +
Adapted from “Object Recognition Versus Object
Discrimination: Comparison Between Human Infants
and Infant Monkeys,” by W. H. Overman,
J. Bachevalier, M. Turner, and A. Peuster, 1992,
Behavioral Neuroscience, 106, p. 18.
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BRAIN DEVELOPMENT AND THE ENVIRONMENT
The development of behaviors is shaped not only by the emergence of brain structures
but also by each person’s environment and experiences. Recall from the discussion of
learning in Chapter 5 that neuroplasticity refers to the lifelong changes in the structure
of the brain that accompany experience. Neuroplasticity suggests that the brain is pliable
and can be molded into different forms, at least at the microscopic level.
Brains exposed to different environmental experiences are molded in different
ways. Culture is an important aspect of the human environment, and so culture must
help to mold the human brain. As noted earlier, we would therefore expect people
raised in widely different cultures to acquire differences in brain structure that have
lifelong effects on their behavior.
The brain is plastic in response not only to external events but also to events within
a person’s body, including the effects of hormones, injury, and abnormal genes. The developing
brain early in life is especially responsive to these internal factors,which in turn
alter the way that the brain reacts to external experiences. In this section, we explore a
whole range of external and internal environmental influences on brain development.
We start with the question of exactly how experience manages to alter brain structure.
Experience and Cortical Organization
Researchers can study the effects of experience on the brain and behavior by placing
laboratory animals in different environments and observing the results. In one of the
earliest such studies, Donald Hebb (1947) took a group of young laboratory rats home
and let them grow up in his kitchen. A control
group grew up in standard laboratory cages at
McGill University.
The “home rats” had many experiences that
the caged rats did not, including being chased
with a broom by Hebb’s less-than-enthusiastic
wife. Subsequently,Hebb gave both groups a ratspecific
“intelligence test” that consisted of learning
to solve a series of mazes, collectively known
as Hebb-Williams mazes. A sample maze is shown
in Figure 6-20. The home rats performed far better
on these tasks than the caged rats did. Hebb
therefore concluded that intelligence must be influenced
by experience.
On the basis of his research, Hebb reasoned
that people reared in “stimulating” environments
In Review .
Children develop increasingly mature motor, language, and cognitive behaviors in predictable
sequences. These behavioral developments correlate with neural changes in the
brain, and neuroscientists infer that the two are probably related. For example, as the cortex
and basal ganglia develop, different motor abilities and cognitive capacities emerge. Although
correlation does not prove causation, correlational research has proved to be powerful
in predicting basic relations between brain development and behavioral milestones.
208 ! CHAPTER 6
S
G
Figure 6-20
Hebb-Williams Maze In
this version of the maze, a
rat is placed in the start
box (S) and must learn to
find the food in the goal
box (G). Investigators can
reconfigure the walls of
the maze to create new
problems. Rats raised in
complex environments
solve such mazes much
more quickly than do rats
raised in standard
laboratory cages.
CH06.qxd 1/28/05 10:14 AM Page 208

will maximize their intellectual development, whereas people raised in “impoverished”
environments will not reach their intellectual potential. Although Hebb’s reasoning
may seem logical, the problem lies in defining in what ways environments may be stimulating
or impoverished.
People living in slums, for example, with few formal educational resources, are not
in what we would normally call an enriched setting, but that does not necessarily mean
that the environment offers no cognitive stimulation or challenge. To the contrary, people
raised in this setting are better adapted for survival in a slum than are people raised in
upper-class homes.Does this adaptability make them more intelligent in a certain way?
In contrast, slum dwellers are not likely to be well adapted for college life,which was
probably closer to what Hebb had in mind when he referred to such an environment as
limiting intellectual potential. Indeed, it was Hebb’s logic that led to the development of
preschool television programs, such as Sesame Street, that offer enrichment for children
who would otherwise have little preschool exposure to reading.
The idea that early experience can change later behavior seems sensible enough,
but we are left with the question of why experience should make such a difference. As
discussed in Chapter 5, one reason is that experience changes the structure of neurons,
which is especially evident in the cortex. Neurons in the brains of animals raised in
complex environments, such as that shown in Figure 6-21A, are larger and have more
synapses than do those of animals reared in barren cages. Representative neurons are
compared in Figure 6-21B.
Presumably, the increased number of synapses results from increased sensory processing
in a complex and stimulating environment. The brains of animals raised in complex
settings also display more (and larger) astrocytes.Although complex-rearing studies
do not address the effects of human culture directly, predictions about human development
are easily made on the basis of their findings.
We know that experience can modify the brain,
and so we can predict that different experiences
might modify the brain differently,which seems to
be the case in language development.
Recall that exposure to different languages
in infancy alters a child’s subsequent ability to
discriminate language-specific speech sounds. A
similar process is likely to take place for music.
People exposed to Western music since childhood
usually find Eastern music peculiar, even nonmusical,
on first encountering it when they are adults.
Presumably, cells in the language- and musicanalysis
systems of the auditory cortex are altered
by early experience and lose much of their plasticity
in adulthood.
This loss of plasticity does not mean that the
adult human brain becomes fixed and unchangeable,
however. Doubtless the brains of adults are
influenced by exposure to new environments and
experiences, although probably more slowly and
less extensively than the brains of children are.
Findings from animal studies have shown plasticity
in the adult brain. In fact, there is evidence that
the brain is affected by experience well into old
age, which is good news for those of us who are
no longer children.
HOW DOES THE BRAIN DEVELOP AND ADAPT? ! 209
Laboratory housed
Complex-environment housed
(A) (B)
Figure 6-21
Enriched Environment, Enhanced
Development (A) A complex housing
environment for a group of about six
rats. The animals have an opportunity
to move about and to interact with
toys that are changed weekly.
(B) Representative neurons from the
parietal cortex of a laboratory-housed
rat (left) and a complex-environmenthoused
rat (right). The neuron on the
right is more complex and has about
25 percent more dendritic space for
synapses.
CH06.qxd 1/28/05 10:14 AM Page 209

Experience and Neural Connectivity
If experience can influence the structure of the cerebral cortex after a person is born,
can it also sculpt the brain prenatally? It can. This prenatal influence of experience is
very clearly illustrated in studies of the developing visual system.
Consider the problem of connecting the eyes to the rest of the developing visual
system.A simple analogy will help. Imagine that students in a large lecture hall are each
viewing the front of the room (the visual field) through a small cardboard tube, such
as an empty paper-towel roll. If each student looks directly ahead, he or she will see
only a small bit of the visual field.
This analogy essentially illustrates how the photoreceptor cells in the eyes act. Each
cell sees only a small bit of the visual field. The problem is to put all the bits together to
form a complete picture. To do so, receptors that see adjacent views (analogously to students
sitting side by side) must send their information to adjacent regions in the various
parts of the brain’s visual system, such as the midbrain.How do they accomplish this feat?
Roger Sperry (1963) suggested that specific molecules exist in different cells in the
various regions of the midbrain, giving each cell a distinctive chemical identity. Each
cell, in other words, has an identifiable biochemical label. This idea is called the
chemoaffinity hypothesis. Presumably, incoming axons seek out a specific chemical,
such as the tropic factors discussed earlier, and consequently land in the correct general
region of the midbrain.
Many experiments have shown this process to take place prenatally as the eye and
brain are developing. But the problem is that chemical affinity “directs” incoming
axons only to a general location. To return to our two adjacent retinal cells, how do they
now place themselves in the precisely correct position?
This is where postnatal experience comes in: fine-tuning of neural placement is believed
to be activity dependent. Because adjacent receptors tend to be activated at the
same time, they tend to form synapses on the same neurons in the midbrain, after
chemoaffinity has drawn them to a general midbrain region. This process is shown in
Figure 6-22. Neurons A and G are unlikely to be activated by the same stimulus, and so
they seldom fire synchronously. Neurons A and B, in contrast, are apt to be activated by
the same stimuli, as are B and C. Through this simultaneous activity over time, cells
eventually line up correctly in the connections that they form.
Now consider what happens to axons coming from different eyes. Although
the neural inputs from the two eyes may be active simultaneously,
cells in the same eye are more likely to be active together than are cells in
different eyes. The net effect is that inputs from the two eyes tend to organize
themselves into neural bands, called columns, that represent the same region
of space in each eye, as shown in Figure 6-23. The formation of these
segregated cortical columns therefore depends on the patterns of coinciding
electrical activity on the incoming axons.
If experience is abnormal—if one eye were covered during a crucial
time in development, for example—then the neural connections will not be
guided appropriately by experience. In fact, this is exactly what happens to
a child who has a “lazy eye.” Visual input from the lazy eye does not contribute
to the fine-tuning of neural connections as it should, and so the details
of those connections do not develop normally, much as if the eye had
been covered. The resulting loss of sharpness in vision known as amblyopia.
The importance of coinciding electrical activity and the formation of
neural columns in the brain are demonstrated beautifully in a clever experiment
by Martha Constantine-Paton (Constantine-Paton & Law, 1978). She
knew that, because the optic nerves of frogs are completely crossed, the optic
tectum on each side has input from only one eye. She wondered what would
210 ! CHAPTER 6
Chemoaffinity hypothesis. Proposal
that neurons or their axons and dendrites
are drawn toward a signaling chemical
that indicates the correct pathway.
Amblyopia. A condition in which vision
in one eye is reduced as a result of
disuse; usually caused by a failure of the
two eyes to point in the same direction.
Time
A
B
F
G
E
C
D
A
B
F
G
E
C
D
Eye
Retina
Optic tectum
in midbrain
Optic tectum
Figure 6-22
Neural Connectivity in the Visual
System Neurons A through G project
from the retina to the tectum in the
midbrain. The activities of adjacent
neurons (C and D, say) are more likely to
coincide than are the activities of widely
separated neurons such as A and G. As a
result, adjacent retinal neurons are more
likely to establish permanent synapses
on the same tectal neurons. By using
chemical signals, axons grow to the
approximate location in the tectum
(top). The connections are made more
precise over time by the correlated
activity (bottom).

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