Ca2+ influx into leech neuropile glial cells mediated by nicotinic acetylcholine receptors

Glia. 1995 Sep;15(1):43-53. doi: 10.1002/glia.440150106.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Carbachol / pharmacology
  • Fluorescence
  • Histocytochemistry
  • Leeches / metabolism*
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Neuroglia / drug effects
  • Neuroglia / metabolism*
  • Nickel / pharmacology
  • Nicotinic Agonists / pharmacology
  • Nicotinic Antagonists / pharmacology
  • Potassium / pharmacology
  • Receptors, Nicotinic / metabolism*
  • Sodium / metabolism

Substances

  • Nicotinic Agonists
  • Nicotinic Antagonists
  • Receptors, Nicotinic
  • Nickel
  • Carbachol
  • Sodium
  • Potassium
  • Calcium