1. Prepared by Jeffrey W. Grimm Western Washington University
PowerPoint Presentation for Biopsychology, 8th 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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Neurodevelopment
Neural development – an ongoing process; the nervous system is plastic
A complex process
Experience plays a key role
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
Beaten, starved, restrained, kept in a dark room, denied normal human interactions
Even with special care and training after rescue, her behavior never became normal
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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6. Induction of the Neural Plate
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
Ectoderm (outermost)
Mesoderm (middle)
Endoderm (innermost)
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7. Induction of the Neural Plate Continued
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 – 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. (Adapted from Cowan, 1979.)
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Neural Proliferation
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 Continued
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, cell body follows
Glial-mediated migration – 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 develping 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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16. 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 9.5 Sperry’s classic study of eye rotation and regeneration.
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18. Axon Growth and Synapse Formation Continued
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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19. Axon Growth and Synapse Formation Continued
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 9.7 The topographic gradient hypothesis. Gradients of ephrin-A and ephrin-B on the developing retina (see McLaughlin, Hindges, & O’Leary, 2003).
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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 – 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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22. Neuron Death and Synapse Rearrangement
~50% 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 survival rate of remaining cells
Increasing number of innervating axons decreases the proportion that survives
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23. Life-Preserving Chemicals
Neurotrophins – promote growth and survival, guide axons, stimulate synaptogenesis
Nerve growth factor (NGF)
Both passive cell death (necrosis) and active cell death (apoptosis)
Apoptosis is safer than necrosis – does not promote inflammation
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24. 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
Ultimately leads to increased selectivity of transmission
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FIGURE 9.8 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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26. Postnatal Cerebral Development in Human Infants
Postnatal growth is a consequence of
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
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27. 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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29. 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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30. 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 9.10 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. (Adapted from Antonini & Stryker, 1993.)
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32. Effects of Experience on Topographic Sensory Cortex Maps
Cross-modal rewiring experiments demon-strate the plasticity of sensory cortexes – with visual input, the auditory cortex can see
Change input, change cortical topography – shifted auditory map in prism-exposed owls
Early music training influences the organization of human auditory cortex – fMRI studies
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33. 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 and this activity is needed for normal development
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34. Neuroplasticity in Adults
The 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
enriched environments and exercise can promote neurogenesis
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FIGURE 9.11 Adult neurogenesis. (Courtesy of Carl Ernst and Brian Christie, Department of Psychology, University of British Columbia.)
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36. Effects of Experience on the Reorganization of the Adult Cortex
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
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37. 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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38. Disorders of Neurodevelopment: Autism Continued
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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39. Disorders of Neurodevelopment: Autism Continued
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
Autistic Savants – intellectually handicapped individuals who display specific cognitive or artistic abilities
~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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40. Genetic Basis of Autism
Siblings of the autistic have a 5% chance of being autistic
60% concordance rate for monozygotic twins
Several genes interacting with the environment
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41. Neural Mechanisms of Autism
Understanding of brain structures involved in autism is still limited, so far implicated:
Cerebellum
Amygdala
Frontal cortex
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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42. Disorders of Neurodevelopment: Williams Syndrome
1 in every 7,500 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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43. Disorders of Neurodevelopment: Williams Syndrome Continued
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 9.13 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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