Ca(2+)-dependent inactivation of P-type calcium channels in nerve terminals

• Published in: Journal of neurochemistry Vol. 62; no. 6; p. 2283
• Main Authors: Tareilus, E, Schoch, J, Breer, H
• Format: Journal Article
• Language: English
• Published: England 01.06.1994
• Subjects: Animals; Calcium - metabolism; Calcium - physiology; Calcium Channels - metabolism; Electrophysiology; Extracellular Space - metabolism; Intracellular Membranes - metabolism; Kinetics; Nerve Endings - metabolism; Rats; Rats, Sprague-Dawley; Signal Transduction; Spectrometry, Fluorescence - methods
• ISSN: 0022-3042
• DOI: 10.1046/j.1471-4159.1994.62062283.x

Rapid Ca2+ signals evoked by K+ depolarization of rat cerebral cortical synaptosomes were measured by dual-channel Ca2+ spectrofluorometry coupled to a stopped-flow device. Kinetic analysis of the signal rise phase at various extracellular Ca2+ concentrations revealed that the responsible voltage-dependent Ca2+ channels, previously identified as P-type Ca2+ channels, inactivate owing to the rise in intracellular Ca2+ levels. At millimolar extracellular Ca2+ concentrations the channels were inactivated very rapidly and the rate was dependent on the high influx rate of Ca2+, thus limiting the Ca2+ signal amplitudes to 500-600 nM. A slower, probably voltage-dependent regulation appears to be effective at lower Ca2+ influx rates, leading to submaximal Ca2+ signal amplitudes. The functional feedback regulation of calcium channels via a sensor for intracellular Ca2+ levels appears to be responsible for the different inhibition characteristics of Cd2+ versus omega-agatoxin IVa.