Development and Plasticity of the Brain

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Author:
goturtlego
ID:
261970
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Development and Plasticity of the Brain
Updated:
2014-03-11 00:27:10
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biological psychology
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psych 261, kalat
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  1. Apoptosis
    • Programmed mechanism of cell death.
    • The postsynaptic synapse stops apoptosis by releasing NGF to the incoming axon. 129
  2. Differentiates
    • Process by which a neuron forms its axon and dendrites.
    • The axon develops first and is towed behind the soma like a tail until reaching its destination.
    • Dendrites develop after migration is complete. 125
  3. Fetal alcohol syndrome
    • Hyperactivity, impulsiveness, difficulty maintaining attention, retardation, facial abnormalities.
    • Alcohol suppresses the release of glutamate and enhances the release of GABA, the main inhibitory transmitter. 130
  4. Focal hand dystonia
    "Musician's cramp", extensive reorganization of the thalamus and cortex leading to touch responses to one finger overlapping those of another. 137
  5. Migrate
    After becoming neuron or glia, cells are guided by immunoglobulins and chemokines to their destinations. 125
  6. Myelination
    Glia (oligodendrocytes and Schwann cells) form myelin in the order of spinal cord, hindbrain, midbrain, and forebrain. 125
  7. Nerve growth factor (NGF)
    Protein released by a muscle which promotes the survival and growth of the axon that has formed a synapse onto it. 129
  8. Neurotrophin
    • Chemical such as NGF which promotes the survival and activity of neurons.
    • Brain-derived neurotrophic factor (BDNF) is the most abundant neurotrophin in the adult cerebral cortex. 130
  9. Proliferation
    • Production of new cells. 
    • Cells lining the ventricles of the brain divide; some remain as stem cells and continue to divide, while others become neurons and glia. 124
  10. Stem cells
    Immature cells. 125
  11. Synaptogenesis
    Formation of synapses. Continues throughout life, but slows in older people. 125
  12. Cerebrovascular accident
    Also stroke. Temporary loss of blood flow into an area. 139
  13. Closed head injury
    • Sharp blow to the head resulting in trauma, but does not puncture the brain.
    • The brain hitting the inside of the skull. 139
  14. Collateral sprouts
    When brain damage results in the loss of a set of axons, the cells that lost their source of innervation releases neurotrophin to induce other axons to branch out and attach to the empty synapses. 142
  15. Deafferented
    It no longer has its afferent (sensory) input. Although the motor nerves still connect to the muscles. 145
  16. Denervation supersensitivity
    • Heightened sensitivity to a neurotransmitter after the destruction of an incoming axon.
    • When damage is extensive, the increased sensitivity can cause chronic pain. 143
  17. Diaschisis
    Decreased activity of surviving neurons after damage to other neurons. 141
  18. Disuse supersensitivity
    Heightened sensitivity as a result of reduced activity in the incoming axon. 143
  19. Edema
    Accumulation of fluid in the brain after stroke which increases pressure and the likelihood of additional strokes. 140
  20. Hemorrhage
    Stroke (or cerebrovascular accident) caused by rupturing of an artery. 139
  21. Ischemia
    Stroke (cerebrovascular accident) caused by blood clot or other obstruction in the artery. 139
  22. Penumbra
    • L. "almost shadow". The region surrounding the immediate damage.
    • When past tPA window, cooling and cannabinoids can still help. 140
  23. Phantom limb
    • Continued sensation of an amputated body part.
    • Only happens when the relevant portion of the somatosensory cortex becomes responsive to alternative input. e.g. when touching face, feel phantom arm. 144
  24. Tissue plasminogen activator (tPA)
    Breaks up blood clots. Best used within 3 hours, unhelpful for hemorrhage. 140

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