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• W2047859904 abstract "Application of FMRFamide (Phe-Met-Arg-Phe-NH2) induced a slow depolarization in neurons of the Aplysia abdominal ganglion. In voltage-clamped cells, FMRFamide induced a slow inward current that increased when the membrane was depolarized beyond −85 mV, showing a negative slope conductance. However, this inward current never reversed to outward current when hyperpolarized beyond the equilibrium potential for K+. The FMRFamide-induced response was markedly augmented in Ca2+-free media, but depressed in Na+-free media. It was unaffected by a change in external potassium. Intracellular injection of guanosine 5′-O-(2-thiodiphosphate) (GDPβS) significantly depressed the FMRFamide response in a dose-dependent way. Injection of cholera toxin (CTX) which did not cause any current response, selectively and irreversibly blocked the FMRFamide response. Neither 3′-deoxyadenosine, an inhibitor of adenylate cyclase, nor H-8, an inhibitor of cyclic adenosine 3′,5′-monophosphate (cyclic AMP)-dependent kinase, depressed the FMRFamide response. 3-Isobutyl-1-methylxanthine (IBMX) did not augment the FMRFamide response appreciably. The FMRFamide response was not occluded at all by a relatively large injection of 8-bromo-cyclic AMP. It was concluded that the FMRFamide response is produced by the opening of the voltage-dependent Na+-channels via activation of a certain CTX-sensitive G-protein which is different from conventional “Gs” that activates adenylate cyclase." @default.
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• W2047859904 date "1992-12-01" @default.
• W2047859904 modified "2023-09-28" @default.
• W2047859904 title "G-protein mediating the slow depolarization induced by FMRFamide in the ganglion cells of Aplysia" @default.
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• W2047859904 doi "https://doi.org/10.1016/0168-0102(92)90046-f" @default.
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