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Chapter 9
Development of the Nervous
System
From Fertilized Egg to You
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Copyright © 2009 Allyn & Bacon
Neurodevelopment
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Neural development – an ongoing
process; the nervous system is plastic
A complex process
Experience plays a key role
Dire consequences when something
goes wrong
Copyright © 2009 Allyn & Bacon
The Case of Genie
What impact does severe deprivation
have on development?
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At age 13, Genie weighed 62 pounds and could
not chew solid food
Beaten, starved, restrained, kept in a dark room,
denied normal human interactions
Can the damage be undone?
Copyright © 2009 Allyn & Bacon
The Case of Genie (continued)
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Genie’s story is often cited for what it tells us
about language development (she only uses
short utterances), but it also illustrates the
impact of abuse on all aspects of behavior
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No response to temperature extremes
Unable to chew
Extremely inappropriate reactions (“silent tantrums”)
Easily terrified
How can neurodevelopment explain this?
Copyright © 2009 Allyn & Bacon
Phases of Development
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Ovum + sperm = zygote
Developing neurons accomplish these
things in five phases
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Induction of the neural plate
Neural proliferation
Migration and aggregation
Axon growth and synapse formation
Neuron death and synapse rearrangement
Copyright © 2009 Allyn & Bacon
Induction of the Neural Plate
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A patch of tissue on the dorsal surface of
the embryo becomes the neural plate
Development induced by chemical signals
from the mesoderm (the “organizer”)
Visible three weeks after conception
Three layers of embryonic cells
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Ectoderm (outermost)
Mesoderm (middle)
Endoderm (innermost)
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Induction of the Neural Plate
(continued)
Neural plate cells are often referred
to as embryonic stem cells
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Have unlimited capacity for self renewal
Can become any kind of mature cell
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Totipotent – earliest cells have the ability
to become any type of body cell
Multipotent – with development, neural
plate cells are limited to becoming one of
the range of mature nervous system cells
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Induction of the
Neural Plate
(continued)
How the neural
plate develops into
the neural tube
during the third
and fourth weeks
of human
embryological
development
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Neural Proliferation
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Neural plate folds to form the neural groove,
which then fuses to form the neural tube
Inside will be the cerebral ventricles and neural
tube
Neural tube cells proliferate in species-specific
ways: three swellings at the anterior end in humans
will become the forebrain, midbrain, and hindbrain
Proliferation is chemically guided by the organizer
areas – the roof plate and the floor plate
Copyright © 2009 Allyn & Bacon
Migration
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Once cells have been created through
cell division in the ventricular zone of
the neural tube, they migrate
Migrating cells are immature, lacking
axons and dendrites
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Migration (continued)
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Two types of neural tube migration
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Two methods of migration
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Radial migration (moving out) – usually by moving
along radial glial cells
Tangential migration (moving up)
Somal – an extension develops that leads
migration, cell body follows
Glial-mediated migration – cell moves along a
radial glial network
Most cells engage in both types of migration
Copyright © 2009 Allyn & Bacon
Migration (continued)
Two types
of neural
migration:
radial
migration
and
tangential
migration
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Migration (continued)
Somal translocation and glia-mediated migration
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Neural Crest
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A structure dorsal to the neural tube and
formed from neural tube cells
Develops into the cells of the peripheral
nervous system
Cells migrate long distances
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Aggregation
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After migration, cells align themselves with
others cells and form structures
Cell-adhesion molecules (CAMs)
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Aid both migration and aggregation
CAMs recognize and adhere to molecules
Gap junctions pass cytoplasm between cells
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Prevalent in brain development
May play a role in aggregation and other
processes
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Axon Growth and Synapse
Formation
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Once migration is complete and structures
have formed (aggregation), axons and
dendrites begin to grow
Growth cone – at the growing tip of each
extension, extends and retracts filopodia as
if finding its way
Chemoaffinity hypothesis – postsynaptic
targets release a chemical that guides
axonal growth, but this does not explain the
often circuitous routes often observed
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Axon Growth
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Mechanisms underlying axonal growth
are the same across species
A series of chemical signals exist along
the way – attracting and repelling
Such guidance molecules are often
released by glia
Adjacent growing axons also provide
signals
Copyright © 2009 Allyn & Bacon
Axon Growth (continued)
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Pioneer growth cones – the first to travel a
route, interact with guidance molecules
Fasciculation – the tendency of developing
axons to grow along the paths established
by preceding axons
Topographic gradient hypothesis – seeks
to explain topographic maps
Copyright © 2009 Allyn & Bacon
Synaptogenesis
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Formation of new synapses
Depends on the presence of glial cells –
especially astrocytes
High levels of cholesterol are needed –
supplied by astrocytes
Chemical signal exchange between pre- and
postsynaptic neurons is needed
A variety of signals act on developing
neurons
Copyright © 2009 Allyn & Bacon
Neuron Death and Synapse
Rearrangement
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~50% more neurons than are needed
are produced – death is normal
Neurons die due to failure to compete
for chemicals provided by targets
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The more targets, the fewer cell deaths
Destroying some cells increases survival
rate of remaining cells
Increasing number of innervating axons
decreases the proportion that survives
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Life-Preserving Chemicals
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Neurotrophins – promote growth and
survival, guide axons, stimulate
synaptogenesis
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Nerve growth factor (NGF)
Both passive cell death (necrosis) and
active cell death (apoptosis)
Apoptosis is safer than necrosis –
“cleaner”
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Postnatal Cerebral Development
in Human Infants
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Postnatal growth is a consequence of
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Synaptogenesis
Myelination – sensory areas and then motor
areas. Myelination of prefrontal cortex continues
into adolescence
Increased dendritic branches
Overproduction of synapses may underlie
the greater plasticity of the young brain
Copyright © 2009 Allyn & Bacon
Development of the Prefrontal
Cortex
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Believed to underlie age-related changes in
cognitive function
No single theory explains the function of this
area
Prefrontal cortex plays a role in working
memory, planning and carrying out
sequences of actions, and inhibiting
inappropriate responses
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Effects of Experience on
Neural Circuits
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Neurons and synapses that are not activated
by experience usually do not survive – use it
or lose it
Humans are uniquely slow in
neurodevelopment – allows for fine-tuning
How do nature and nurture interact to modify
the early development, maintenance, and
reorganization of neural circuits?
Copyright © 2009 Allyn & Bacon
Early Studies of Experience
and Neurodevelopment
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Early visual deprivation
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Fewer synapses and dendritic spines in primary
visual cortex
Deficits in depth and pattern vision
Enriched environment
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Thicker cortexes
Greater dendritic development
More synapses per neuron
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Competitive Nature of Experience and Neurodevelopment
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Monocular deprivation changes the
pattern of synaptic input into layer IV of
V1 (but not binocular deprivation)
Altered exposure during a sensitive
period leads to reorganization
Active motor neurons take precedence
over inactive ones
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How Experience Might
Influence Neurodevelopment
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Many possibilities
Neural activity regulates the expression
of genes that direct the synthesis of
CAMs
Neural activity influences the release of
neurotrophins
Some neural circuits are spontaneously
active and this activity is needed for
normal development
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Neuroplasticity in Adults
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Mature brain changes and adapts
Neurogenesis (growth of new neurons)
seen in olfactory bulbs and
hippocampuses of adult mammals –
adult neural stem cells created in the
ependymal layer lining in ventricles and
adjacent tissues
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Effects of Experience on Adult
Cortex Reorganization
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Tinnitus (ringing in the ears) – produces
major reorganization of primary auditory
cortex
Adult musicians who play instruments
fingered by left hand have an enlarged
representation of the hand in the right
somatosensory cortex
Skill training leads to reorganization of
motor cortex
Copyright © 2009 Allyn & Bacon
Autism
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Three core symptoms
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Reduced ability to interpret emotions and
intentions
Reduced capacity for social interaction
Preoccupation with a single subject or activity
Intensive behavioral therapy may improve
function
Heterogenous – level of brain damage and
dysfunction varies
Copyright © 2009 Allyn & Bacon
Autism (continued)
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Incidence: 6.6 per 1,000 births (or 1 in 166)
80% males, 60% mentally retarded, 35% epileptic,
25% have little or no language ability
Most have some abilities preserved – rote memory,
jigsaw puzzles, musical ability, artistic ability
Savants – intellectually handicapped individuals
who display specific cognitive or artistic abilities
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~1/10 autistic individuals display savant abilities
Perhaps a consequence of compensatory functional
improvement in one area following damage to another
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Genetic Basis of Autism
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Siblings of the autistic have a 5% chance of being
autistic
60% concordance rate for monozygotic twins
Several genes interacting with the environment
Thalidomide – given early in pregnancy – increases
chance of autism
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Indicates neurodevelopmental error in first weeks of
pregnancy as cranial nerve motor neurons develop
Consistent with deficits in control of face, mouth, eye
movements, and with abnormal ear structure
Evidence for a role of a gene on chromosome 7
Copyright © 2009 Allyn & Bacon
Neural Mechanisms of Autism
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Widespread damage, especially to
cerebellum and associated brain stem
structures
Two lines of research
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Abnormal response to faces in autistic
patients
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Spend less time than non-autistic subjects
looking at faces, especially eyes
Low fMRI activity in fusiform face area
Possibly deficient in mirror neuron function
Copyright © 2009 Allyn & Bacon
Williams Syndrome
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~1 in every 20,000 births
Mental retardation and an uneven pattern of
abilities and disabilities
Sociable, empathetic, and talkative – exhibit
language skills, music skills, and an
enhanced ability to recognize faces
Profound impairments in spatial cognition
Usually have heart disorders associated with
a mutation in a gene on chromosome 7 – the
gene (and others) is absent in 95% of those
with Williams
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Williams Syndrome (continued)
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Evidence for a role of chromosome 7 (as in
autism)
General thinning of cortex at juncture of
occipital and parietal lobes, and at the
orbitofrontal cortex
“Elfin” appearance – short, small upturned
noses, oval ears, broad mouths
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cells differentiate together contracting
Rat Heart
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