Preferential inhibition of omega-conotoxin-sensitive presynaptic Ca2+ channels by adenosine autoreceptors.
Adenosine is a potent modulator of transmitter release at a variety of synapses. The adenosine A1 receptor is assumed to reside in presynaptic terminals and to function as a negative autoreceptor. How adenosine reduces transmitter release is uncertain; it may reduce the calcium influx during nerve terminal depolarization by either activating K+ currents or inhibiting Ca2+ currents, although other mechanisms have been proposed. We have directly measured intracellular Ca2+ concentrations of giant pre-synaptic terminals in the chick ciliary ganglion. We report here that adenosine inhibited the nerve-evoked Ca2+ influx in the terminal by activating A1 receptors. Reduced Ca2+ influx was due largely to inhibition of omega-conotoxin GVIA-sensitive Ca2+ channels in the presynaptic terminal.
Department of Physiology, Kyoto University Faculty of Medicine, Japan.
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Yawo
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Chuhma
D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects* / Q000378:metabolism; D002642:Chick Embryo; D005724:Ganglia / Q000187:drug effects / Q000378:metabolism; D010455:Peptides / Q000494:pharmacology; D011983:Receptors, Purinergic / Q000187:drug effects* / Q000378:metabolism; D013570:Synaptic Membranes / Q000187:drug effects / Q000378:metabolism; D020960:omega-Conotoxins
D015220:Calcium Channels; D010455:Peptides; D011983:Receptors, Purinergic; D020960:omega-Conotoxins; C053423:Conus magus toxin; D000241:Adenosine; D002118:Calcium