Ca2+ influx into leech neuropile glial cells mediated by nicotinic acetylcholine receptors.
The effect of cholinergic agonists and antagonists on the intracellular free Ca2+ concentration ([Ca2+]i) of leech neuropile glial cells was investigated by use of iontophoretically injected fura-2. In neuropile glial cells, cholinergic agonists induced a marked increase in [Ca2+]i that was inhibited by d-tubocurarine, alpha-bungarotoxin, strychnine, and atropine. The efficacy of the various agonists and antagonists indicates that the [Ca2+]i increase is mediated by the nicotinic acetylcholine (ACh) receptors that have been characterized previously in these cells by using electrophysiological methods. In the presence of high agonist concentrations, [Ca2+]i partly recovered, suggesting that the ACh receptors desensitize. The [Ca2+]i increase induced by cholinergic agonists was abolished in Ca2(+)-free solution, which indicates that it is caused by Ca2+ influx from the external medium. The agonist-induced [Ca2+]i increase was partly preserved in Na(+)-free solution, whereas the agonist-induced membrane depolarization was strongly suppressed. The agonist-induced [Ca2+]i increase was also partly preserved in the presence of 5 mM Ni2+, which almost abolished the K(+)-induced [Ca2+]i increase mediated by voltage-dependent Ca2+ channels. It is concluded that at low agonist concentrations the [Ca2+]i increase in leech neuropile glial cells is mediated exclusively by the ion channels associated with the nicotinic ACh receptors. At high agonist concentrations, voltage-dependent [Ca2+]i increase in leech neuropile glial cells is mediated exclusively by the ion channels associated with the nicotinic ACh receptors. At high agonist concentrations, voltage-dependent Ca2+ channels activated by the concomitant membrane depolarization also contribute to the agonist-induced Ca2+ influx.
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Institut für Neurobiologie, Heinrich-Heine-Universität Düsseldorf, Germany.
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D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D005453:Fluorescence; D006651:Histocytochemistry; D007865:Leeches / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism*; D009532:Nickel / Q000494:pharmacology; D018722:Nicotinic Agonists / Q000494:pharmacology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011978:Receptors, Nicotinic / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism
D018722:Nicotinic Agonists; D018733:Nicotinic Antagonists; D011978:Receptors, Nicotinic; D009532:Nickel; D002217:Carbachol; D012964:Sodium; D011188:Potassium; D002118:Calcium