D-amphetamine-elicited action potential bursts in central snail neurons: role of second messenger systems

Neuronal bursts of action potentials are closely related to seizure activity. Amphetamine rarely induces seizures at therapeutic doses, but seizure may occur after the first dose. This study investigated factors affecting d-amphetamine-elicited action potential bursts in isolated central snail neurons.

The central right parietal neuron 1 (RP1 neuron) from the subesophageal ganglia of the African snail Achatina fulica Ferussac was used to evaluate neurotransmitter systems involved in d-amphetamine-elicited potential burst activity by use of conventional electrophysiological and general pharmacological techniques.

d-Amphetamine (135 and 270 microM) elicited bursts of action potentials in the RP1 neuron in a concentration dependent manner. The burst activity was not blocked by pretreatment with prazosin (100 microM), yohimbine (100 microM), propranolol (100 microM), atropine (1 mM), or by continuous perfusion of calcium-free solution. These results suggest that the burst activity elicited by d-amphetamine was not due to activation of the cholinergic or adrenergic receptors of the excitable membrane. The burst firing of action potentials was decreased following extracellular application of the specific protein kinase A inhibitors H89 (N-[2-(p-bromocinnamylamino)-ethyl]-5-isoquinoline sulfonamide, 10 microM), or KT-5720 (10 microM). However, the burst firing of action potentials was not affected after extracellular application of the specific protein kinase C inhibitors Ro 31-8220 (10 microM) or chelerythrine (10 microM). Forskolin (10 microM), an activator of adenylyl cyclase, facilitated the burst firing of action potentials elicited by d-amphetamine. However, in the absence of d-amphetamine, a higher concentration of forskolin (100 microM) was able to elicit burst firing of action potentials.

These results suggest that the action potential bursts elicited by d-amphetamine are associated with the cyclic adenosine monophosphate (cAMP) second messenger system and are not related to the cholinergic or adrenergic receptors or protein kinase C activity in the RP1 snail neuron.