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Intracellular calcium and its sodium‐independent regulation in voltage‐clamped snail neurones.

1. We have used both Ca(2+)‐sensitive microelectrodes and fura‐2 to measure the intracellular free calcium ion concentration ([Ca2+]i or its negative log, pCai) of snail neurones voltage clamped to ‐50 or ‐60 mV. Using Ca(2+)‐sensitive microelectrodes, [Ca2+]i was found to be approximately 174 nM and pCai, 6.76 +/‐ 0.09 (mean +/‐ S.E.M.; n = 11); using fura‐2, [Ca2+]i was approximately 40 nM and pCai, 7.44 +/‐ 0.06 (mean +/‐ S.E.M., n = 10). 2. Depolarizations (1‐20 s) caused an increase in [Ca2+]i which was abolished by removal of extracellular Ca2+, indicating that the rise in [Ca2+]i was due to Ca2+ influx through voltage‐activated Ca2+ channels. 3. Caffeine (10‐20 mM) caused an increase in [Ca2+]i in the presence or absence of extracellular Ca2+. The effects of caffeine on [Ca2+]i could be prevented by ryanodine. 4. Thapsigargin, an inhibitor of the endoplasmic reticulum Ca(2+)‐ATPase, caused a small increase in resting [Ca2+]i and slowed the rate of recovery from Ca2+ loads following 20 s depolarizations. 5. Neither replacement of extracellular sodium with N‐methyl‐D‐glucamine (NMDG), nor loading the cells with intracellular sodium, had any effect on resting [Ca2+]i or the rate of recovery of [Ca2+]i following depolarizations. 6. The mitochondrial uncoupling agent carbonyl cyanide m‐chlorophenylhydrazone (CCmP) caused a small gradual rise in resting [Ca2+]i. Removal of extracellular sodium during exposure to CCmP had no further effect on [Ca2+]i. 7. Intracellular orthovanadate caused an increase in resting [Ca2+]i and prevented the full recovery of [Ca2+]i following small Ca2+ loads, but removal of extracellular sodium did not cause a rise in [Ca2+]i. We conclude that there is no Na(+)‐Ca2+ exchanger present in the cell body of these neurones and that [Ca2+]i is maintained by an ATP‐dependent Ca2+ pump.