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Lecture 9

Neurodevelopment.docx


Department
Psychology
Course Code
PSYC 2410
Professor
Elena Choleris
Lecture
9

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NEURODEVELOPMENT
Development of the Central Nervous System
About the CNS we used to think that:
Embryonic developmentPostnatal-Childhood DevelopmentThen in adulthood a stable
“fixed” organ
Now we know that:
The Central Nervous System continues to change throughout our entire lifeBrain
Plasticity
A More Comprehensive View:
Embryonic Development Postnatal/Childhood Development in adulthood a plastic
organ
Throughout: genes environment
e.g. environment in utero. Postnatal experienes
After formation cells need to:
1. Differentiate (e.g. muscle cells, liver cells, neurons, glia)
2. Migrate to the appropriate location
3. Establish functional relation with other cells
Key Steps of Cellular Differentiation
Totipotent: early embryonic cells, can differentiate in any cell type of the body
Pluripotent: initial differentiation. Cells can still become many, but not all, cell types
Multipotent: cells that can develop into multiple cell types within a class of cells (e.g.
neural cells)
Unipotent: cells that can only complete their differentiation into one cell type
Totus=all; Multi=many; Pluri=many
Stem Cells: two properties
1. Unlimited divisions without differentiation
2. Potential to differentiate into different cell types
a) Totipotent stem cells
b) Pluripotent stem cells
c) Multipotent neural or glial stem cells
d) Etc.
Embryonic Development of the Central Nervous System
1. Induction of the Neural Plate
2. Neural Proliferation
3. Migration and Aggregation
4. Axon Growth and Synapse Formation
5. Neuron Death and Synapse Rearrangement
1. Induction of the Neural Plate
Ectoderm, Mesoderm, Endoderm
Neural Plate
Neural Groove
Neural Tube
Central Canal + Neural Crest
Induction: mesoderm  neural plate

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NEURODEVELOPMENT
2. Neural Proliferation
After the closure of the neural tube
Mostly in the ventricular zone
Species-specific sequences
Regulated by chemical signals from the floor plate (along ventral surface) and roof plate
(dorsal surface of the neural tube)
3. Migration and Aggregation
1. Glial Mediated Locomotion
2. Somal Translocation
Guided by chemicals that either attract or repel migrating cells
Cell-adhesion molecules (CAMs): on the surface of cells  migration, recognition, and
adhesion
Gap junctions (connexins-connexon)
Neuron Migration Disorders
Kallmann Syndrome: abnormal genitals and dysfunctional sense of smell related to failed
migration of neurons secreting sex hormones and coding for odors. Genetic mutation
related to CAMs
Dyslexia and Schizophrenia: neural migration errors implicated…
Lissencephaly: “smooth brain” – severe mental retardation
4. Axon Growth and Synpase Formation
Growth Cone: at the top of a growing axon, it extends and retracts filopodia (finger-like
processes)
Chemoaffinity Hypothesis
Target-specific chemical labels
Hypothesis supported by: in vitro studies (no spatial cues, only chemical)
Discovery of several such Chemical labels
Sperry’s classic study of eye rotation and regeneration
When an insect is dangled in front of a normal frog, the frog strikes at it accurately with
its tongue.
When the eye is rotated 180 degrees without cutting the optic nerve, the frog misdirects
its strike by 180 degrees.
When the optic nerve is cut and the eye is rotated by 180 degrees, at first the frog is blind;
but once the optic nerve has regenerated, the frog misdirects its strikes by 180 degrees.
This is because the axons of the optic nerve, although rotated, grow back to their original
synaptic sites.
Note: the frog optic tectum is homologous to the mammalian superior colliculus.
Note: retinal ganglion cells regeneration doesn’t occur in mammals

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NEURODEVELOPMENT
Chemoaffinity Hypothesis NOT supported by:
1. Targets transplanted in new positions can become incorrectly innervated.
Example.
Thigh – calf – foot. Thigh – Thigh – calf – foot
The second thigh acquires calf innervation
2. It is often the case that the route to the target is circuitous, rather than linear
Chemoaffinity Hypothesis. A revision
CAMs  Chemical Trials  Pioneer Growth Cones
Subsequent growth cones follow the pioneer growth cones
Supported by Fasciculation
Topographic Gradient Hypothesis
Two intersecting gradients (up-down and left-right) of chemicals on the originating tissue
guide axonal growth from one topographic array (such as a retina) to another (the optic
tectum)
Hypothesis supported by:
Maintenance of Topographic integrity
Axons normally grow from the frog retina and terminate on the optic tectum in an orderly
fasion. The assumption that this orderliness results from point-to-point chemoaffinity is
challenged by the following two observations:
1. When Half the retinal was destroyed and the optic nerve cut, the retinal ganglion
cells from the remaining half retina projected systematically over the entire
tectum
2. When half the optic tectum was destroyed and the optic nerve cut, the retinal
ganglion cells from the retina projected systematically over the remaining half of
the optic tectum
4. Synapse Formation = Synaptogenesis
Synaptogenesis  neuron-neuron chemical “talk”
Another key role for glial cells (astrocytes)
1. In vitro studies: neuron cultured with astrocytes form 7 times as many synapses as
those without astrocytes
2. In vivo studies: synapse-promoting and inhibiting signals interact
Functions of Neuronal Death
1. Neurons that make incorrect connections die. Developing neurons are very
promiscuous. Make lots of connections; not all are essential
2. New neurons make more focused synapses  cell death increases overall accuracy
of synaptic connections
5. Neuron Death
Apoptosis: ACTIVE process of cell death. A “CLEAN” process
Necrosis: PASSIVE cell death. A “DIRTY” process
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