Regulation of calcium influx into buccal muscles of Aplysia by acetylcholine and serotonin.
Acetylcholine (ACh) causes contraction of Aplysia buccal muscles E1 and I5, and serotonin (5-hydroxytryptamine, 5-HT) enhances ACh-elicited contractions of these muscles. Possible roles of calcium influx in mediating these responses were examined by studying influx of 45Ca++. 5-HT increased calcium influx into both I5 and E1. Maximal influx occurred at 10(-6) M 5-HT and the increased influx could be sustained in the presence of 5-HT for at least 10 min. ACh also caused calcium influx, and calcium influx increased approximately in proportion to log[ACh] from 10(-5) M to 10(-3) M ACh. 5-HT and ACh probably bring about calcium influx by different mechanisms since the effect of ACh was additive to a maximal 5-HT response, and 10(-4) M hexamethonium bromide inhibited the increased influx caused by ACh but did not affect influx caused by 5-HT. Cyclic AMP analogues and forskolin neither caused an increase in calcium influx nor an increase in the influx caused by ACh. The data support a model in which ACh-elicited contractions of I5 and E1 are due primarily to calcium entry across the extracellular membrane, and 5-HT can "load" an intracellular site by a mechanism different from that activated by ACh. The data do not support a role for cyclic AMP in mediating the calcium influx response to 5-HT.
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D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D001048:Aplysia; D002118:Calcium / Q000378:metabolism*; D000242:Cyclic AMP / Q000502:physiology; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials; D009119:Muscle Contraction; D009132:Muscles / Q000294:innervation*; D011985:Receptors, Serotonin / Q000502:physiology; D012701:Serotonin / Q000502:physiology*
D007473:Ion Channels; D011985:Receptors, Serotonin; D012701:Serotonin; D000242:Cyclic AMP; D000109:Acetylcholine; D002118:Calcium