1. Prepared by Jeffrey W. Grimm Western Washington University
PowerPoint Presentation for Biopsychology, 9th Edition by John P.J. Pinel
Prepared by Jeffrey W. Grimm
Western Washington University
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2. From Fertilized Egg to You
Chapter 9
Development of the
Nervous System
From Fertilized Egg to You
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Learning Objectives
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 -
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Neurodevelopment
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
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
Ovum + Sperm = Zygote
Developing neurons accomplish these things in five phases.
Induction of the neural plate
Neural proliferation
Migration and aggregation
Axon growth and synapse formation
Neuron death and synapse rearrangement
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7. Induction of the Neural Plate
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
Ectoderm (outermost)
Mesoderm (middle)
Endoderm (innermost)
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8. Induction of the Neural Plate (Con’t)
Neural plate cells are often referred to as embryonic stem cells.
Have Unlimited Capacity for Self-Renewal
Can Become Any Kind of Mature Cell
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
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
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)
Two Types of Neural Tube Migration
Radial migration (moving out): usually by moving along radial glial cells
Tangential migration (moving up)
Two Methods of Migration
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
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
After migration, cells align themselves with others cells and form structures.
Cell-Adhesion Molecules (CAMs)
Aid both migration and aggregation
CAMs recognize and adhere to molecules.
Gap junctions pass cytoplasm between cells.
Prevalent in brain development
May play a role in aggregation and other processes
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17. Axon Growth and Synapse Formation
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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20. Axon Growth and Synapse Formation (Con’t)
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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21. Axon Growth and Synapse Formation (Con’t)
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
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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24. Neuron Death and Synapse Rearrangement
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.
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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25. Life-Preserving Chemicals
Neurotrophins promote growth and survival, guide axons, and stimulate synaptogenesis.
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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26. Synapse Rearrangement
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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28. Postnatal Cerebral Development in Human Infants
Postnatal growth is a consequence of:
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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29. Development of the Prefrontal Cortex
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
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.
Critical period
Sensitive period
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31. Early Studies of Experience and Neurodevelopment
Early Visual Deprivation
Fewer synapses and dendritic spines in primary visual cortex
Deficits in depth and pattern vision
Enriched Environment
Thicker cortexes
Greater dendritic development
More synapses per neuron
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32. Competitive Nature of Experience and Neurodevelopment
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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34. Effects of Experience on Topographic Sensory Cortex Maps
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 prism-exposed owls.
Early music training influences the organization of human auditory cortex: fMRI studies.
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35. Experience Fine-Tunes Neurodevelopment
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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36. Neuroplasticity in Adults
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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38. Effects of Experience on the Reorganization of the Adult Cortex
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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39. Disorders of Neurodevelopment: Autism
Three Core Symptoms
Reduced ability to interpret emotions and intentions
Reduced capacity for social interaction
Preoccupation with a single subject or activity
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40. Disorders of Neurodevelopment: Autism (Con’t)
Intensive behavioral therapy may improve function.
Heterogenous: level of brain damage and dysfunction varies
Often Considered a Spectrum Disorder
Autism spectrum disorders
Asperger’s syndrome
Mild autism spectrum disorder in which cognitive and linguistic functions are well preserved
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41. Disorders of Neurodevelopment: Autism (Con’t)
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
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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42. Genetic Basis of Autism
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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43. Neural Mechanisms of Autism
Understanding of brain structures involved in autism is still limited; so far, research has implicated:
Cerebellum
Amygdala
Frontal cortex
There are two lines of research on cortical involvement in autism.
Abnormal response to faces in autistic patients
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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44. Disorders of Neurodevelopment: Williams Syndrome
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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45. Disorders of Neurodevelopment: Williams Syndrome (Con’t)
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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