Muscarinic receptor activation modulates ligand-gated ion channels in an insect motoneuron via changes in intracellular calcium

An isolated ganglion preparation has been used to make recordings from an identified cockroach neuron in situ. We have shown that the magnitude of conductance increase of ligand-gated ion channels produced by agonists can be modulated by activation of muscarinic ACh receptors (mAChRs); currents through nicotinic ACh receptors (nAChRs) are suppressed, while GABA currents can be either enhanced or suppressed. mAChR activation causes a rise in [Ca2+](i) measured using the fluorescent Ca2+ indicator fluo-3. This rise in [Ca2+](i) appears to trigger modulation of nicotinic ACh and GABA currents, since the effects of mAChR activation are mimicked by brief increases in [Ca2+](i) produced by flash photolysis of the Ca2+ chelator nitr-5. These modulatory effects outlast the rise in [Ca2+](i) evoked by mAChR activation or photolytic Ca2+ release by 5-10 min. The prolongation by Li+ of the modulatory effects mediated by mAChRs suggests a possible involvement of the phosphoinositol pathway. These results indicate that mAChRs acting via intracellular messengers can exert a powerful modulatory influence upon nACh or GABA gated ion channels of neurons in which these receptors are co-localized.