Muscarinic receptor agonist-induced increases in cytosolic Ca2+ concentrations in chick ciliary ganglion cells

Masaru Sorimachi, Katsutoshi Furukawa, Yumiko Abe, Norio Akaike

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


We used fura-2 microfluorometry to examine the mechanism underlying the muscarinic receptor agonist-induced increase in the cytosolic Ca2+ concentration ([Ca]in) in acutely isolated chick ciliary ganglion neurons. The order of potencies of muscarinic agonists in increasing [Ca]in was: oxotremorine M > muscarine > methacholine > oxotremorine > bethanechol. The muscarine-induced increase in [Ca]in persisted after treatment with thapsigargin, which blocked caffeine- and muscarinic agonist-induced Ca2+ release. The muscarine-sensitive [Ca]in increase was inhibited by both L- and N-type Ca2+ channel blockers but potentiated by an L-type Ca2+ channel agonist. Muscarine was effective in increasing [Ca]in in the presence of a desensitizing concentration of nicotine, and simultaneous addition of maximal doses of muscarine and nicotine caused an additive increase in [Ca]in. On the other hand, nicotine-, ATP-, and high K+-induced increase in [Ca]in was markedly potentiated during continuous stimulation with muscarine. These results suggest that muscarinic receptor stimulation increases Ca2+ influx passing through voltage-dependent Ca2+ channels. However, the muscarine-induced Mn2+ influx was observed in only some muscarine-sensitive cells, suggesting that muscarine-induced depolarization is too weak to overcome the inhibitory effect of Mn2+ on Ca2+ channels.

Original languageEnglish
Pages (from-to)67-75
Number of pages9
JournalBrain research
Issue number1-2
Publication statusPublished - 1995 Oct 23


  • Ca channel antagonist
  • Ciliary ganglion cell
  • Fura-2 microfluorometry
  • Mn influx
  • Muscarine
  • Nicotine

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology


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