Abstract

Octopamine was found to decrease extrajunctional, but not junctional glutamate responses, in mealworm neuromuscular preparations. This action of octopamine was mimicked by forskolin, 8-(4-chlorophenylthio)-adenosine 3′:5′-cyclic monophosphate (CPT-cyclic AMP), and 8-bromoguanosine 3′:5′-cyclic monophosphate (8-bromo-cyclic GMP), but not by 1,2-oleoylacetylglycerol (OAG), a protein kinase C activator. We suggest that the octopamine-induced reduction in the glutamate sensitivity of extrajunctional membranes may enable the muscle to more closely follow its neuronal input by preventing a depolarization (and hence a conductance increase) due to the discharge of unsequestered transmitter molecules at nonsynaptic sites.

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