Abstract
The Ca 2+ permeability of a nicotinic acetylcholine receptor (nAChR) in the rat CNS was determined using both current and fluorescence measurements on medial habenula neurons. The elementary slope conductance of the nAChR channel was 11 pS in pure external Ca 2+ (100 mM) and 42 pS in standard solution. Ca 2+ influx through nAChRs resulted in the rise of cytosolic Ca 2+ concentration ([Ca 2+] i) to the micromolar range. This increase was maximal under voltage conditions (below −50 mV) in which Ca 2+ influx through voltage-activated channels was minimal. Ca 2+ influx through nAChRs directly activated a Ca 2+-dependent Cl − conductance. In addition, it caused a decrease in the GABA A response that outlasted the rise in [Ca 2+] i. These results underscore the physiological significance of Ca 2+ influx through nAChR channel in the CNS.
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