Protein Information

ID 342
Name acetylcholine receptor (protein family or complex)
Synonyms Acetylcholine receptor; Acetylcholine receptors

Compound Information

ID 336
Name strychnine
CAS strychnidin-10-one

Reference

PubMed Abstract RScore(About this table)
8847100 Hochstrate P, Schlue WR: Ca2+ influx into leech neuropile glial cells mediated by nicotinic acetylcholine receptors. Glia. 1995 Sep;15(1):43-53.
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.
1(0,0,0,1)