Attenuation in central neurons: its relationship to increased intracytoplasmic free calcium, calcium binding and memory storage.
A mechanism responsible for attenuation of dendritic spikes of nucleus reticularis gigantocellularis (NRG) origin was addressed. Stimulation of afferent neurons with pulses of 100 per sec frequency generated attenuation in specific neurons. Intrasomatic infusion of EGTA reversed the attenuation. The results suggest that attenuation results from intracytoplasmic accumulation of free Ca2+ due to differences in rate of Ca influx and Ca binding. This accumulation generates a concentration dependent prevention of Ca2+ (and Na+) influx that causes the attenuation. The free intracytoplasmic Ca2+ is removed mainly by binding on proteins and/or polypeptides, a mechanism that promotes memory storage.
D000818:Animals; D001933:Brain Stem / Q000502:physiology*; D002118:Calcium / Q000378:metabolism*; D002415:Cats; D003593:Cytoplasm / Q000378:metabolism; D003712:Dendrites / Q000502:physiology; D004533:Egtazic Acid / Q000494:pharmacology; D005260:Female; D008297:Male; D008568:Memory; D008839:Microelectrodes; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D012964:Sodium / Q000378:metabolism
D004533:Egtazic Acid; D012964:Sodium; D002118:Calcium