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POWERPOINT PRESENTATION
FOR BIOPSYCHOLOGY,
9TH EDITION
BY JOHN P.J. PINEL
P R E PA R E D B Y J E F F R E Y W. G R I M M
WESTERN WASHINGTON UNIVERSITY
COPYRIGHT © 2014 PEARSON EDUCATION, INC.
ALL RIGHTS RESERVED.
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Chapter 9
Development of the
Nervous System
From Fertilized Egg to You
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Learning Objectives
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LO1: Describe the 5 phases of neurodevelopment.
LO2 The human brain is not fully developed at birth. Explain.
LO3: Discuss 5 examples of experience affecting early mammalian
development.
LO4: Discuss 5 examples of experience affecting adult mammalian
development.
LO5: Describe autism and attempts to identify its neural
mechanisms.
LO6: Describe WIlliams syndrome and attempts to identify its neural
mechanisms.
Video - https://www.youtube.com/watch?v=lhapeOo6laA
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Neurodevelopment
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Neural development is an ongoing process;
the nervous system is plastic.
A Complex Process
Experience plays a key role.
There are dire consequences when
something goes wrong.
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The Case of Genie
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At age 13, Genie weighed 62 pounds and
could not chew solid food.
She had been beaten, starved, restrained,
kept in a dark room, and denied normal
human interactions.
Even with special care and training after
rescue, her behavior never became normal.
The case of Genie illustrates the impact of
severe deprivation on development.
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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
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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 is 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
(Con’t)
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Neural plate cells are often referred to as
embryonic stem cells.
Have Unlimited Capacity for Self-Renewal
Can Become Any Kind of Mature Cell
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Totipotent: the 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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FIGURE 9.1 How the neural plate
develops into the neural tube during
the third and fourth weeks of human
embryological development. (Based
on Cowan, 1979.)
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Neural Proliferation
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The 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.
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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 (Con’t)
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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; the cell body follows.
Glial-mediated migration: the cell moves along a
radial glial network.
Most cells engage in both types of migration.
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FIGURE 9.2 The two types of
neural migration: radial
migration and tangential
migration.
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FIGURE 9.3 Two methods by which cells
migrate in the developing neural tube:
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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FIGURE 9.4 Growth cones. The
cytoplasmic fingers (the filopodia)
of growth cones seem to grope for
the correct route. (Courtesy of
Naweed I. Syed, Ph.D., Departments
of Anatomy and Medical Physiology,
the University of Calgary.)
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FIGURE 9.5 Sperry’s classic study
of eye rotation and regeneration.
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Axon Growth and
Synapse Formation (Con’t)
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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.
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Axon Growth and
Synapse Formation (Con’t)
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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.
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FIGURE 9.6 The regeneration of the optic nerve of the frog after
portions of either the retina or the optic tectum have been
destroyed. These phenomena support the topographic gradient
hypothesis.
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Synapse Formation
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Formation of new synapses depends on the
presence of glial cells—especially
astrocytes.
High levels of cholesterol are needed—and
are supplied by astrocytes.
Chemical signal exchange between pre- and
postsynaptic neurons is needed.
A variety of signals act on developing
neurons.
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Neuron Death and Synapse
Rearrangement
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Approximately 50 percent 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 the survival
rate of remaining cells.
Increasing the number of innervating axons
decreases the proportion that survive.
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Life-Preserving Chemicals
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Neurotrophins promote growth and
survival, guide axons, and 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 because
it does not promote inflammation.
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Synapse Rearrangement
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Neurons that fail to establish correct
connections are particularly likely to die.
Space left after apoptosis is filled by
sprouting axon terminals of surviving
neurons.
This ultimately leads to increased
selectivity of transmission.
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FIGURE 9.7 The effect
of neuron death and
synapse rearrangement
on the selectivity of
synaptic transmission.
The synaptic contacts
of each axon become
focused on a smaller
number of cells.
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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 of 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.
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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 the
Early Development, Maintenance,
and Reorganization of Neural Circuits
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Permissive experiences: those that are
necessary for information in genetic
programs to be manifested
Instructive experiences: those that
contribute to the direction of development
Effects of experience on development are
time-dependent.
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Critical period
Sensitive period
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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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Ocular Dominance Columns Example:
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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FIGURE 9.9 The effect of a few days of early monocular
deprivation on the structure of axons projecting from
the lateral geniculate nucleus into layer IV of the
primary visual cortex. Axons carrying information from
the deprived eye displayed substantially less branching.
(Based on Antonini & Stryker, 1993.)
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Effects of Experience on
Topographic Sensory
Cortex Maps
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Cross-modal rewiring experiments demonstrate
the plasticity of sensory cortexes—with visual
input, the auditory cortex can see.
Change the input, and you change the cortical
topography: e.g., shifted auditory map in prismexposed owls.
Early music training influences the organization of
human auditory cortex: fMRI studies.
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Experience Fine-Tunes
Neurodevelopment
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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; this activity is needed for normal
development.
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Neuroplasticity in Adults
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The mature brain changes and adapts.
Neurogenesis (growth of new neurons) is
seen in the olfactory bulbs and
hippocampuses of adult mammals: adult
neural stem cells created in the ependymal
layer lining in ventricles and adjacent
tissues.
Enriched environments and exercise can
promote neurogenesis.
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FIGURE 9.10 Adult neurogenesis.
The top panel shows new cells in the
dentate gyrus of the hippocampus—
the cell bodies of neurons are
stained blue, mature glial cells are
stained green, and new cells are
stained red. The bottom panel shows
the new cells from the top panel
under higher magnification, which
makes it apparent that the new cells
have taken up both blue and red
stain and are thus new neurons.
(Courtesy of Carl Ernst and Brian
Christie, Department of Psychology,
University of British Columbia.)
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Effects of Experience on the
Reorganization of the
Adult Cortex
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Tinnitus (ringing in the ears) produces
major reorganization of the primary
auditory cortex.
Adult musicians who play instruments
fingered by the left hand have an enlarged
representation of that hand in the right
somatosensory cortex.
Skill training leads to reorganization of
motor cortex.
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Disorders of
Neurodevelopment: 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
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Disorders of Neurodevelopment:
Autism (Con’t)
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Intensive behavioral therapy may improve
function.
Heterogenous: level of brain damage and
dysfunction varies
Often Considered a Spectrum Disorder
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Autism spectrum disorders
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Asperger’s syndrome
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Mild autism spectrum disorder in which cognitive and
linguistic functions are well preserved
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Disorders of Neurodevelopment:
Autism (Con’t)
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Incidence: 6.6 per 1,000 Births (or 1 in 166)
80 percent of those affected are males, 60 percent
are mentally retarded, 35 percent are epileptic, and
25 percent have little or no language ability.
Most have some abilities preserved: e.g., rote
memory, jigsaw puzzles, musical ability, or artistic
ability.
Autistic savants: intellectually handicapped
individuals who display specific cognitive or artistic
abilities
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Approximately 1 in 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 percent
chance of being autistic
There is a 60 percent concordance rate
for monozygotic twins.
Several Genes Interacting with the
Environment
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Neural Mechanisms of Autism
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Understanding of brain structures involved
in autism is still limited; so far, research
has implicated:
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Cerebellum
Amygdala
Frontal cortex
There are two lines of research on cortical
involvement in autism.
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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
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Disorders of Neurodevelopment:
Williams Syndrome
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1 in Every 7,500 Births
Mental Retardation and an Uneven Pattern of
Abilities and Disabilities
People with Williams syndrome are sociable,
empathetic, and talkative; they exhibit language
skills, music skills, and an enhanced ability to
recognize faces.
Profound Impairments in Spatial Cognition
Those with Williams syndrome usually have heart
disorders associated with a mutation in a gene
on chromosome 7; the gene (and others) is
absent in 95 percent of those with Williams.
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Disorders of Neurodevelopment:
Williams Syndrome (Con’t)
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There is 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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FIGURE 9.12 Two areas of reduced cortical volume and
one area of increased cortical volume observed in
people with Williams syndrome. (See Meyer-Lindenberg
et al., 2006; Toga & Thompson, 2005.)
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