CHAPTER 5

DEVELOPMENT AND PLASTICITY OF THE BRAIN

Chapter Outline
I. The Development of the Brain

A. Maturation of the Vertebrate Brain

1. The human central nervous system begins to form when the embryo is about 2 weeks old.
2. A neural tube forms around a fluid-filled cavity; this structure eventually sinks under the skin
surface and develops into the hindbrain, midbrain, and forebrain. The fluid-filled cavity becomes
the central canal and the four ventricles.
3. The human brain weighs approximately 350 grams at birth and around 1,000 grams at one year of
age. The average adult brain weighs between 1,200 and 1,400 grams.
B. Growth and Development of Neurons
The five steps of neuron development:
a. Proliferation: Production of new cells; cells along the ventricles of the brain divide to
become neurons and glia.
b. Migration: Movement of primitive neurons and glia toward their final destination in the
brain. Chemicals known as immunoglobins and chemokines guide the new cells to their
eventual destination in the brain.
c. Differentiation: Neurons develop an axon and dendrites (this distinguishes neurons from
other cells in the body); the axon grows before the dendrites, while the neuron is migrating
toward its destination.
d. Myelination: Glia cells produce myelin sheaths around axons which allow for rapid
transmission. In humans, myelin forms first in the spinal cord before forming in the brain.
Myelination begins during the prenatal period and continues into adulthood.
e. Synaptogenesis: Formation of synapses. This is the last step in neural development and
continues throughout life.
C. New Neurons Later in Life
1. The traditional belief was that adult vertebrate brains gain all their neurons during early
development and could only lose neurons later in life.
2. The differentiation of stem cells (undifferentiated cells) in the olfactory bulb and hippocampus are
an exception to the traditional belief—but in general new neurons do not form in other parts of the
adult mammalian brain.
D. Pathfinding by Axons
1. Sperry (1943) discovered that severed optic nerve axons will grow back to their original targets in
the tectum. He showed that this process was dependent on chemical gradients in the target cells by
severing the optic nerve and rotating the eye by 180°.
2. For example, TOPDV is a protein 30 times more concentrated than ventral retina neurons in the
axons of the dorsal retina, and is 10 times more concentrated in the ventral tectum than it is in the
dorsal tectum. Retinal axons and tectal cells with high concentrations of TOPDV connect to each
other; those with the lowest concentrations do likewise.
E. Competition Among Axons as a General Principle
1. Postsynaptic cells strengthen the synapses of some cells and weaken synapses with others.
2. Neural Darwinism: During development, synapses form randomly before a selection process
keeps some and rejects others (this is only partly accurate since synapse formation is also
influenced by chemical guidance and neurotrophic factors).
F. Determinants of Neuron Survival
1. While working on the sympathetic ganglion, Rita Levi-Montalcini discovered that muscles that
synapse with the axons from the ganglia don’t determine how many neurons are produced but
which synapses survive.
2. She discovered that muscles produce and release nerve growth factor (NGF), which promotes
the survival and growth of axons.
3. Axons that don’t receive enough NGF degenerate and their cell bodies die. All neurons are born
with this suicide program and will automatically die if the right synaptic connection is not made.
This programmed cell death is called apoptosis.
4. Neurotrophin: a chemical (like NGF) that promotes the survival and activity of neurons. In
addition to NGF, the brain also uses brain-derived neurotrophic factor (BDNF) as a neurotrophin.
BDNF is the most abundant neurotrophin in the adult mammalian cortex.
5. Initially, all areas of the developing nervous system produce far more neurons than will survive
into adulthood. This loss of cells is a natural part of development.
6. After maturity, the apoptotic process becomes dormant and neurons do not need neurotrophins to
survive. Neurotrophins are used in adult brains to increase branching of axons and dendrites
throughout life. Deficiencies of neurotrophins lead to cortical shrinking and are linked to several
brain diseases.
G. The Vulnerable Developing Brain
1. Compared to the mature brain, the developing brain is more vulnerable to malnutrition, toxic
chemicals, and infections.
2. Fetal alcohol syndrome (FAS): Caused by alcoholic consumption during pregnancy. Symptoms
include decreased alertness, hyperactivity, facial abnormalities, mental retardation, motor
problems, and heart defects.
3. Prenatal exposure to cocaine can lead to slight decreases in IQ scores and somewhat greater
decreases in language skills.
4. Prenatal exposure to cigarette smoking is associated with attention deficit/ hyperactivity disorder
(ADHD), aggression, and impaired memory and intelligence.
5. Stress to the mother has also been found to cause academic and social problems for her offspring.
H. Differentiation of the Cortex
1. Neurons in different parts of the cortex have different shapes.
2. Ultimate shape of neurons and functions of regions depend on input received.
3. In immature ferrets, researchers rerouted the optic nerve on one side of the brain away from its
normal thalamic target onto a thalamic target that usually gets input from the ears. They found that
the parts of the thalamus and cortex that formerly received auditory information reorganized to
process visual information.
I. Fine-tuning by Experience
1. Because of the unpredictability of life, we have evolved the ability to redesign our brain (within
limits) in response to experience.
2. Experience and Dendritic Branching
a. Environmental enrichment leads to a thicker cortex, more dendritic branching and improved
performance on learning tasks in rats.
b. Much of the benefit of enriched environments in rats is simply due to activity. Increased size
expansion of neurons has also been demonstrated in humans as a function of physical activity.
c. Enriched environments enhance sprouting of axons and dendrites in a wide variety of species
including humans.
3. Effects of Special Experiences
a. People blind from birth are better at discriminating between objects by touch and have
increased activation in their occipital cortex (visual cortex) while performing this task. Further
research using magnetic stimulation to inactivate brain areas demonstrated that blind people
 use the occipital cortex to discriminate between tactile stimuli and Braille symbols but sighted
people do not. Similar results are also found using verbal stimuli.
b. Extensive practice of a particular skill makes a person more adept at that skill. In a few cases,
researchers have identified brain changes that are associated with increased expertise at a
particular skill. For example:
 The auditory cortex response to pure tones is twice as large for professional musicians as
for nonmusicians. Moreover, a part of the temporal cortex was found to be 30% larger in
professional musicians.
 Violin players have a larger area devoted to the left fingers in the postcentral gyrus than
nonmusicians.
4. When Brain Reorganization Goes Too Far
a. Typically expanded cortical representation of personally important information is beneficial.
However, in extreme cases the reorganization creates problems.
b. Focal hand dystonia (musician’s cramp): this happens in musicians who practice extensively
when the expanded representation of each finger overlaps its neighbor. The fingers become
clumsy, fatigue easily, and make involuntary movements that interfere with the desired task.
A similar condition called “writer’s cramp” can happen to people who spend all day writing.

II. Plasticity After Brain Damage

A. Brain Damage and Short-Term Recovery

1. Brain damage can result from a number of causes, including tumors, infections, exposure to
radiation or toxic substances, and degenerative conditions such as Parkinson’s and Alzheimer’s
disease.
2. Closed head injury: A sharp blow to the head that does not actually puncture the brain. The most
common cause of brain damage in young people. Closed head injuries damage the brain because
of rotational forces that drive the brain tissue against the inside of the skull.
3. Reducing the Harm From a Stroke.
a. Stroke (cerebrovascular accident): A temporary loss of blood flow to the brain. This is a
common cause of brain damage, especially in the elderly.
 Ischemia: The most common type of stroke; loss of blood flow caused by a blood clot or
other obstruction of an artery.
 Hemorrhage: A less common type of stroke; bleeding due to the rupture of an artery.
 Ischemia and hemorrhage lead to common problems including edema (fluid
accumulation), increased potassium levels due to dysfunctional sodium-potassium
pumps, and increased release of glutamate.
 Decreasing cell death after a stroke can be accomplished by administering tissue
plasminogen activator (tPA) clot-busting drugs, that restore blood flow following
ischemia or by using drugs that antagonize glutamate activity.
 Additional cells in the penumbra (the area that surrounds the immediate damage) can be
saved by opening potassium channels to reduce overstimulation.
 However, researchers have discovered that the most effective method for decreasing cell
death in animals is to lower brain temperature from 37C to 29C within 30 minutes after
the ischemic episode occurs.
B. Later Mechanisms of Recovery
1. Increased Brain Stimulation
a. Diaschisis: Decreased activity of surviving neurons after other neurons are destroyed. Behavioral
deficits due to diaschisis can sometimes be improved with the use of stimulant drugs.
2. Regrowth of Axons: Under certain circumstances, damaged axons can grow back. However,
regeneration is minimal in the mature mammalian central nervous system, possibly because of a
large amount of scar tissue or the secretion of growth-inhibiting chemicals.
3. Sprouting: Sprouting is a normal condition, as the brain is constantly adding new branches of
axons and dendrites and withdrawing old ones. This process accelerates in response to damage.
a. Collateral sprouts: A newly formed branch from an uninjured axon. The collateral sprouts
attach to a synapse vacated when the original axon was destroyed. This process is initiated by
neurotrophins secreted by the cells that have lost their source of innervation.
4. Denervation supersensitivity: Heightened sensitivity to a neurotransmitter after the destruction
of incoming axons. Heightened sensitivity as a result of inactivity by an incoming axon is called
disuse supersensitivity.
a. Mechanisms of supersensitivity include increased numbers of receptors and increased
effectiveness of receptors.
b. Denervation supersensitivity is a way of compensating for decreased input. However, the
increased sensitivity can lead to intense responses in normal inputs, which can result in
prolonged pain.
c. People with brain damage generally show some behavioral improvement after the damage.
This recovery is due to structural changes in the surviving neurons and learned changes in
behavior.
5. Reorganized Sensory Representations and the Phantom Limb
a. Visual cortex is remapped following loss of neurons from the upper left visual field.
b. Monkeys that had an entire limb deafferented twelve years previously had a large portion of
their cerebral cortex (which was previously responsive to that limb) become responsive to the
face. It was later found that amputation of a limb results in axonal sprouts forming not only in
the cortex, but also in the spinal cord, brainstem, and thalamus.
c. Brain scans confirm that this process often leads to a phantom limb, a continuing sensation
of an amputated body part.
d. The brain remains plastic throughout life.
6. Learned Adjustments in Behavior: Much of the recovery after brain damage is learned; the
individual makes better use of unimpaired abilities. A brain-damaged person or animal may also
learn to use abilities that at first appear lost, but are only impaired. For example:
a. Monkeys with a deafferented (loss of sensory or afferent nerves from a body part) limb fail
to use it because walking on three limbs is apparently easier than trying to move the impaired
limb. However, if forced, they can learn to use the deafferented limb.
Key Terms
apoptosis fetal alcohol syndrome penumbra
closed head injury focal hand dystonia phantom limb
collateral sprout hemorrhage proliferation
deafferent ischemia stem cells
denervation supersensitivity migration stroke (cerebrovascular
diaschisis myelination accident)
differentiation nerve growth factor (NGF) synaptogenesis
disuse supersensitivity neural Darwinism tissue plasminogen activator
edema neurotrophin (tPA)