Abstract
In the presence of 0.5 mM EGTA (a calcium chelator), the muscarinic agonist carbachol at 0.1 mM inhibited octopamine-stimulated cyclic AMP (cAMP) production in intact ventral nerve cords of Periplaneta americana. This effect was reduced by the addition of 0.1 mM atropine (a muscarinic antagonist), suggesting that the effect is mediated via muscarinic acetylcholine receptors (mAChR). This inhibitory effect of carbachol was not observed in the synaptosomes of nerve cords, suggesting that the inhibitory effect was not due to direct coupling of the mAChR to adenylate cyclase but mediated by other second messengers. The inhibitory effect seems to be due to an increase in the intracellular calcium level. In the presence of exogeneous extracellular 0.25 mM Ca2+ the octopamine-stimulated cAMP production was lower than that in the absence of extracellular Ca2+, and the cAMP levels were not further reduced by adding carbachol to the octopamine-stimulated cAMP production system. Washing did not remove all of the inhibitory activity of carbachol in intact nerve cords, indicating that carbachol modulated octopaminergic neurotransmission irreversibly.
