PSY 3061 Lecture Notes - Lecture 14: Nmda Receptor, Excitotoxicity, Memory Consolidation
Document Summary
Occurs mostly in alcohol withdrawal (binge, withdrawal, binge, withdrawal, etc. [alcohol (ethanol) is a gaba agonist: during alcohol intoxication, alcohol opens gaba receptors ad enables hyperpolarization of glutamatergic neurons by allowing cl- influx, allows influx of negatively charged ions. [alcohol (ethanol) is an nmda receptor antagonist: during alcohol intoxication, alcohol blocks ca2+ ions from entering glutamatergic neurons, especially in the hippocampus, alcohol binds to glycine site, and blocks entrance of calcium ions (stops the. [glutamate-induced excitotoxicity from repeated alcohol withdrawal: first-time alcohol use, nmda receptor (nmdar) is blocked by ethanol, postsynaptic glutamatergic excitability is inhibited, repeated alcohol use, glutamatergic neurons are less sensitive to glutamate because there are so many. Moderate levels of glutamate release will stimulate much more than it normally would (at a larger scale): glutamate activates the postsynaptic neuron too much, causing an unsafe amount of. In very high levels of postsynaptic ca2+, apoptotic genes (genes that activate apoptosis) will be expressed and the cell will die.
