PSYC414 Lecture Notes - Lecture 1: Ionotropic Glutamate Receptor, Neurotransmitter, Brain Ischemia
13 Mar 2018
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Document Summary
High levels of glutamate can be toxic to nerve cells. Retinal damage in rats w/ sodium salt of glutamic acid. Injured hypothalamus, arcuate nucleus role in controlling endocrine system: msg induced damage to this structure stunted growth, obesity, etc. If injected directly, could lesion that structure: damage at post synaptic sites, also seen in other excitatory amino acids. Excitotoxicity hypothesis excessive exposure to glutamate and related excitatory amino acids are caused by prolonged depolarization of receptive neurons leading to damage/death. Ingesting large amounts of excitatory amino acid domoic acid: made up of marine algae, passed via eating tainted food, neurological symptoms. Brain ischemia also seen in excitotoxic brain damage interruption of blood flow to the brain: stroke or heart attack, massive release of glutamate in affected area prolonged nmda receptor activation. Glutamate = fast excitatory signaling in ns. Numerous glutamatergic pathways (i. e. , projections of pyramidal neurons of cerebral cortex, parallel fibers of cerebellar cortex, and w/in hc)
