1. Pre-natal & Post-natal Development & Neuroplasticity Ch. 9

2. Outline 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

3. 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

4. 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

5. 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

6. Copyright © 2006 by Allyn and Bacon

7. 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

8. 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)

9. 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

10. 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

11. Copyright © 2006 by Allyn and Bacon

13. 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

14. 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

15. 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

16. Chemoaffinity Hypothesis The target of each growing axon has a specific chemical that draws the correct growing axon to it

17. 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

18. 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 left- right) of chemicals on the originating tissue (the retina in this case)

19. Copyright © 2006 by Allyn and Bacon

20. 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

21. 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

22. 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:

23. 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

24. 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”?)

25. 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

26. 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

27. 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)

28. 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

29. 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

30. 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

31. Effects of Experience on Neurodevelopment Simply placing an adult animal in an enriched environment can increase neurogenesis in brain regions such as the hippocampus

32. 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

33. 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

34. Biopsychology of Psychiatric Disorders Ch. 18

35. Outline Schizophrenia –Symptoms and Etiology –Antischizophrenic Drugs

36. Psychiatric Disorders Psychiatric disorder is a psychological disorder that is severe enough that it requires treatment by a clinical psychologist or a psychiatrist

37. Psychiatric Disorders Psychiatric disorders involve more subtle pathology than neuropsychological disorders Influenced by experiential factors like stress

38. 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

39. Symptoms of Schizophrenia Bizarre delusions, hallucinations, inappropriate affect, incoherent thoughts, or odd behavior (catatonia or echolalia)

40. Symptoms of Schizophrenia

41. 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

42. 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

43. 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

44. 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