G-protein mediating the slow depolarization induced by FMRFamide in the ganglion cells of Aplysia.
Neurosci Res
; 15(4): 255-64, 1992 Dec.
Article
en En
| MEDLINE
| ID: mdl-1283779
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 Ca(2+)-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) (GDP beta S) 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.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Aplysia
/
Neuropéptidos
/
Neurotransmisores
/
Proteínas de Unión al GTP
/
Ganglios
/
Fármacos Neuromusculares Despolarizantes
/
Neuronas
Límite:
Animals
Idioma:
En
Revista:
Neurosci Res
Asunto de la revista:
NEUROLOGIA
Año:
1992
Tipo del documento:
Article
País de afiliación:
Japón