Muscarinic receptor agonist-induced increases in cytosolic Ca2+ concentrations in chick ciliary ganglion cells
Sorimachi, M.; Furukawa, K.; Abe, Y.; Akaike, N.
Brain Research 696(1-2): 67-75
1995
ISSN/ISBN: 0006-8993 PMID: 8574686 DOI: 10.1016/0006-8993(95)00772-i
Accession: 009064793
We used fura-2 microfluorometry to examine the mechanism underlying the muscarinic receptor agonist-induced increase in the cytosolic Ca-2+ concentration ((Ca)-in) in acutely isolated chick ciliary ganglion neurons. The order of potencies of muscarinic agonists in increasing (Ca)-in was: oxotremorine M gt muscarine gt methacholine gt oxotremorine gt bethanechol. The muscarine-induced increase in (Ca)-in persisted after treatment with thapsigargin, which blocked caffeine- and muscarinic agonist-induced Ca-2+ release. The muscarine-sensitive (Ca)-in increase was inhibited by both L- and N-type Ca channel blockers but potentiated by an L-type Ca-2+ 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 Ca-2+ influx passing through voltage-dependent Ca-2+ channels. However, the muscarine-induced Mn-2+ influx was observed in only some muscarine-sensitive cells, suggesting that muscarine-induced depolarization is too weak to overcome the inhibitory effect of Mn-2+ on Ca-2+ channels.