Transcript Development & Neuroplasticity - U

Pre-natal & Post-natal Development
& Neuroplasticity
Ch. 9
Outline
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Induction of the Neural Plate
Neural Proliferation
Migration and Aggregation
Axon Growth and Formation of Synapses
Neural Death and Synapse Rearrangement
Postnatal Cerebral Development in Humans
Effects of Experience of Neurodevelopment
Neuroplasticity
Induction of The Neural Plate
• After 3 weeks of conception, a patch of
ectoderm (tissue that becomes skin or
neuron) on the dorsal surface of the embryo
becomes distinguishable; this patch is the
neural plate which eventually develops
into the nervous system
Induction of The Neural Plate
• Prior to induction of the neural plate, the
cells are undifferentiated (able to be
transplanted to a new site in the embryo and
develop in the same way as cells at the new
site); these are called stem cells
• However, after induction, cells are destined
to become a neuron
Induction of The Neural Plate
• The neural plate develops into the neural
groove and then into the neural tube,
which subsequently develops into the CNS.
By 40 days, the anterior end of the tube
develops 3 swelling that become the
forebrain, midbrain, and hindbrain
Copyright © 2006 by Allyn and
Bacon
Neural Proliferation
• After the neural tube is formed, the
developing nervous system cells rapidly
increase in number
• Cell division occurs in the ventricular zone
of the neural tube; when they leave the cell
division cycle, cells migrate into other
layers
Migration and Aggregation
• Cells migrate away from the ventricular zone
along a temporary network of radial glial cells,
which are present in only the developing neural
tube
• The cells of the neocortex migrate in an inside-out
pattern; the deepest layers form first so that the
cells of the superficial layers must migrate through
them (like lava out of a volcano)
Migration and Aggregation
• Migration of the cells of the neural crest is
of particular interest because these cells
ultimately form the PNS, and thus may have
a long way to migrate
Migration and Aggregation
• Neural crest cells transplanted to a new part of the
neural crest migrate to the destination that is
appropriate for cells in the new location; thus the
migration routes must be encoded in the
medium through which they travel rather than
in the cells themselves; many different types of
chemical signals have been found that guide the
migration of the axons of future PNS neurons
Copyright © 2006 by Allyn and
Bacon
Migration and Aggregation
• Once migration is complete, cells must aggregate
correctly to form various neural structures; this is
hypothesized to be mediated by specialized neural
cell adhesion molecules in the cell membranes
(NCAMs)
• decrease in number of NCAMs is one underlying
factor of schizophrenia
– migrating cells cannot travel full distance to outer
layers where they belong
Axon Growth and
the Formation of Synapses
• Once the aggregation of developing neurons
is complete, axons and dendrites grow out
from the neurons; growing to the correct
target is particularly difficult for axons that
have a long way to grow
Axon Growth and
the Formation of Synapses
• Accurate axon growth seems to be directed
by a growth cone at the growing axon tip
• Three hypotheses have been proposed to
explain how growth cones make their way
to correct destination:
– Chemoaffinity hypothesis
– Blueprint hypothesis
– Topographic-gradient hypothesis
Chemoaffinity Hypothesis
• The target of each growing axon has a
specific chemical that draws the correct
growing axon to it
Blueprint Hypothesis
• The substrate contains physical and
chemical trails that growth cones follow to
their correct destinations
• Only first axon has to reach correct target;
others appear to follow the pioneer growth
cone’s route
Topographic-Gradient
Hypothesis
• Axon growth from one topographic array
(such as a retina) to another (the optic
tectum) is guided by the relative position of
cell bodies and terminals on two
intersecting gradients (up-down and leftright) of chemicals on the originating tissue
(the retina in this case)
Copyright © 2006 by Allyn and
Bacon
Axon Growth and
the Formation of Synapses
• Summary: all of the evidence on axon
growth and regeneration suggests that a
variety of mechanisms can guide axon
growth; the growth of different axons
appears to be guided by different
combinations of these mechanisms
Neuron Death and
Synapse Rearrangement
• Up to 50% of neurons that develop die
during the course of normal development;
the fact that neurons that make incorrect
connections are more likely to die suggests
that cell death increases the overall
accuracy of synaptic connections
Neuron Death and
Synapse Rearrangement
• Three lines of evidence suggest that neurons
die because they fail to compete
successfully for some life-preserving factor
supplied by their target:
Neuron Death and
Synapse Rearrangement
(1) Implantation of an extra target site
decreases neuron death
(2) Destroying some neurons before the
period of neuron death increases the
survival rate of the remainder
(3) Increasing the number of axons that
initially synapse on a target decreases
survival rate of the remainder
Postnatal Cerebral Development
in Humans
• The human brain develops more slowly
than other species, not maturing until late
adolescence
• In particular, the prefrontal cortex
(reasoning) is the last part of the brain to
reach maturity, and it is thought to mediate
many higher cognitive abilities (is this why
teenagers make “bad decisions”?)
Postnatal Growth of
The Human Brain
• Brain volume quadruples between birth
and adulthood; most of this increase in
volume comes from increased numbers of
synapses (synaptogenesis), myelination of
axons, and increased dendritic branching
Postnatal Growth of
The Human Brain
• Synaptogenesis is assumed to indicate
increased analytic ability in a brain region;
synaptogenesis in the visual cortex peaks at
about 4 months postnatal, whereas in
prefrontal cortex maximal density is
reached in the second year
Postnatal Growth of
The Human Brain
• Myelination increased the speed of of axonal
conduction; again sensory and motor areas are
myelinated in the first few months of life while the
prefrontal cortex is not fully myelinated until
adolesence
• Many synapses that form early in development are
eventually lost; overproduction of synapses in the
young brain may contribute to its greater
plasticity (capability for functions to be mediated
by other neurons not originally involved)
Development of
Prefrontal Cortex
• Parallels the course of human cognitive
development
• Linked to three main types of cognitive function:
working memory, or the ability to keep
information accessible for short periods of time;
planning and completing sequences of actions;
and inhibiting inappropriate responses
• Damage leads to perseverative errors in adults
(Wisconsin Card Sorting Task), so that their
behavior looks more like infants
Effects of Experience on
Neurodevelopment
• Neurodevelopment results from an
interaction between neurons and their
environment
• Neurons and synapses that are not
activated by experience do not usually
survive
Effects of Experience on
Neurodevelopment
• Experience alters neural development in at
least 3 different ways: (1) by influencing
gene expression for cell adhesion
molecules; (2) by influencing the release of
neurotrophins (3) and by altering the
spontaneous activity of certain brain regions
Effects of Experience on
Neurodevelopment
• Simply placing an adult animal in an
enriched environment can increase
neurogenesis in brain regions such as the
hippocampus
Plasticity in Adults
• It has only been recently appreciated that
the adult brain is capable of considerable
plasticity
• Neurogenesis has been demonstrated in the
hippocampus, olfactory bulb, and
association cortex
Plasticity in Adults
• There is also evidence for functional
reorganization of cortex in adult
vertebrates, including humans
• For example, repeated active identification
of somatosensory stimuli can expand the
representation of the areas that are
stimulated in the somatosensory
homunculus
Biopsychology of Psychiatric
Disorders
Ch. 18
Outline
• Schizophrenia
– Symptoms and Etiology
– Antischizophrenic Drugs
Psychiatric Disorders
• Psychiatric disorder is a psychological
disorder that is severe enough that it
requires treatment by a clinical psychologist
or a psychiatrist
Psychiatric Disorders
• Psychiatric disorders involve more subtle
pathology than neuropsychological
disorders
• Influenced by experiential factors like
stress
Schizophrenia
• Schizophrenia is characterized by a
complex and diverse set of symptoms that
often overlap with other forms of mental
illness and may change over time
Symptoms of Schizophrenia
• Bizarre delusions, hallucinations,
inappropriate affect, incoherent thoughts,
or odd behavior (catatonia or echolalia)
Symptoms of Schizophrenia
Etiology of Schizophrenia
• Genetic basis - concordance rate of
schizophrenia in identical twins is about
45%; in fraternal twins or siblings 10%
• Regions of several different chromosomes
have been implicated in the vulnerability to
schizophrenia
Etiology of Schizophrenia
• In addition to genetic predisposition,
experiences such has prenatal trauma,
infection, and stress may all be
susceptibility factors
• Thus, individuals inherit a predisposition
for schizophrenia which may or may not be
activated by experience
Antischizophrenic Drugs
• Chlorpromazine was initially developed as
an antihistamine
• Noticed side-effect was calmness
• After being administered for three weeks, it
calmed agitated schizophrenics and caused
catatonic schizophrenics to become more
active
Antischizophrenic Drugs
• Reserpine (snake root plant) is also an
effective drug for reducing schizophrenic
symptoms
• However, it is no longer used because it
lowers blood pressure to dangerous levels