Bursting firing of action potentials in central snail neurons elicited by d-amphetamine: role of the electrogenic sodium pump.

The effects of d-amphetamine on central neurons were studied electrophysiologically in the identifiable RP4 neuron of the African snail, Achatina fulica Ferussac. d-Amphetamine elicited bursting activity from the central RP4 neuron in a concentration-dependent manner. The bursting activity was not blocked in a high magnesium (30 mM) medium, or after a continuous perfusion of propranolol, prazosin, haloperidol, phenobarbital, hexamethonium, d-tubocurarine, atropine, or calcium-free solution containing EDTA or verapamil. These results suggested that the bursting activity elicited by d-amphetamine was not due to: (1) the synaptic effects of neurotransmitters; or (2) the cholinergic or adrenergic receptors of the excitable membrane. However, the bursting activity elicited by d-amphetamine was blocked in the presence of ouabain or in the medium containing potassium-free, low sodium solutions. d-Amphetamine did not elicit the bursting activity of the LP4 neuron in the same ganglia preparation, and did not alter the GABA-elicited currents of the snail neuron. It is concluded, therefore, that d-amphetamine induced a potassium- and sodium-dependent bursting activity of central neurons. The bursting activity of the central neuron may be associated with the sodium pump of the neuron.