In the African giant snail, Achatina fulica Férussac, the ionic mechanisms underlying slow depolarization of a heart excitatory neurone, PON, induced by the activity of two cerebral ganglionic neurones, d-RCDN and d-LCDN, were investigated under voltage-clamp. The slow depolarization of PON that was induced by the activity of the cerebral neurones was blocked by the serotonin (5-HT) antagonist, methysergide. Bath application of 5-HT to the axotomized PON produced a similar slow depolarization, which was also blocked by methysergide. These results suggest that the neurotransmitter of d-RCDN and d-LCDN is 5-HT. Under voltage-clamp, activity of the cerebral neurones usually produced an inward shift in the holding current of PON with a decrease of conductance. Ionic substitution experiments and injection of Cs+ into PON showed that the response was mainly due to a decrease in K+ conductance. In some cases, this inward shift showed two components: an early component with increased conductance and a late one with decreased conductance. The early component was not decreased by Cs+ injection but was augmented by EGTA injection into PON, which may suggest the involvement of a Ca2+ conductance in this synaptic response. Application of 5-HT produced a similar inward shift in holding current which was also mainly the result of a decrease in the background K+ current. 5-HT was also found to increase the voltage-dependent Ca2+ current and the inward rectifying K+ current. The significance of these results is discussed in relation to the heart regulation of this snail.
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Furukawa et al. (1988) studied this question.
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