Development and Plasticity of the Brain
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- Programmed mechanism of cell death.
- The postsynaptic synapse stops apoptosis by releasing NGF to the incoming axon. 129
- 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
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
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
After becoming neuron or glia, cells are guided by immunoglobulins and chemokines to their destinations. 125
Glia (oligodendrocytes and Schwann cells) form myelin in the order of spinal cord, hindbrain, midbrain, and forebrain. 125
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
- 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
- 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
Immature cells. 125
Formation of synapses. Continues throughout life, but slows in older people. 125
Also stroke. Temporary loss of blood flow into an area. 139
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
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
It no longer has its afferent (sensory) input. Although the motor nerves still connect to the muscles. 145
- Heightened sensitivity to a neurotransmitter after the destruction of an incoming axon.
- When damage is extensive, the increased sensitivity can cause chronic pain. 143
Decreased activity of surviving neurons after damage to other neurons. 141
Heightened sensitivity as a result of reduced activity in the incoming axon. 143
Accumulation of fluid in the brain after stroke which increases pressure and the likelihood of additional strokes. 140
Stroke (or cerebrovascular accident) caused by rupturing of an artery. 139
Stroke (cerebrovascular accident) caused by blood clot or other obstruction in the artery. 139
- L. "almost shadow". The region surrounding the immediate damage.
- When past tPA window, cooling and cannabinoids can still help. 140
- 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
Tissue plasminogen activator (tPA)
Breaks up blood clots. Best used within 3 hours, unhelpful for hemorrhage. 140
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