Abstract

The role of the intracellular second messengers on the bursting firing of action potentials in central snail neurons elicited by d-amphetamine was studied in the identified RP4 neuron of the African snail Achatina fulica Ferussac. Oscillation of membrane potential and bursting firing of action potentials were elicited by d-amphetamine in a concentration dependent manner. The bursting firing of action potentials was decreased following extracellular application of (1) H8 ( N-(2-methyl-amino) ethyl-3-isoquinoline sulphonamide dihydrochloride), a specific protein kinase A inhibitor and (2) anisomycin, a protein synthesis inhibitor. However, the bursting firing of action potentials were not affected after (1) extracellular application of H7 (1,(5-isoquinolinesulphonyl)-2-methylpiperasine dihydrochloride), a specific protein kinase C (PKC) inhibitor, or (2) intracellular application of GDP βS, a G protein inhibitor. The oscillation of membrane potential of the bursting activity was blocked after intracellular injection of 3′-deoxyadenosine, an adenylyl-cyclase inhibitor. These results suggested that the bursting firing of action potentials elicited by d-amphetamine in snail neurons may be associated with the cyclic adenosine monophosphate (cAMP) second messenger system; on the other hand it may not be associated with the G protein and protein kinase C activity.

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