TY - JOUR
T1 - Muscarinic receptor agonist-induced increases in cytosolic Ca2+ concentrations in chick ciliary ganglion cells
AU - Sorimachi, Masaru
AU - Furukawa, Katsutoshi
AU - Abe, Yumiko
AU - Akaike, Norio
N1 - Funding Information:
This study was supported by Grand-in-Aid for Scientific Research (No. 05808076 to M.S.) from the Ministry of Education, Science and Culture, Japan.
PY - 1995/10/23
Y1 - 1995/10/23
N2 - 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.
AB - 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.
KW - Ca channel antagonist
KW - Ciliary ganglion cell
KW - Fura-2 microfluorometry
KW - Mn influx
KW - Muscarine
KW - Nicotine
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U2 - 10.1016/0006-8993(95)00772-I
DO - 10.1016/0006-8993(95)00772-I
M3 - Article
C2 - 8574686
AN - SCOPUS:0028806155
VL - 696
SP - 67
EP - 75
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
IS - 1-2
ER -