Abstract

The roles of the ionic currents in the firing of potential bursts elicited by d-amphetamine in central snail neurons were studied in the identified RP4 neuron of the African snail, Achatina fulica Ferussac, using the two-electrode voltage-clamp method. Oscillations of membrane potential bursts were elicited by d-amphetamine. The action potential bursts elicited by d-amphetamine decreased following intracellular injection of either EDTA or magnesium, or extracellular application of lanthanum. Voltage-clamped studies revealed that d-amphetamine decreased the fast Na +, Ca 2+ and transient outward K + currents of the RP4 neuron. It also decreased the steady-state K + current and elicited a negative slope resistance in the steady-state I–V curve between −50 and −10 mV. The amplitude of negative slope resistance was decreased if either Na +-free saline or Co 2+-substituted Ca 2+-free saline was perfused. d-Amphetamine did not increase the amplitude of the slowly inactivating Ca 2+ current or the persistent Na + currents of RP4 neuron. Tetraethylammonium, a blocker of the delayed outward K + current, elicited action potential bursts and negative slope resistance in the RP4 neuron, while 4-aminopyridine, an inhibitor of transient outward K + current (I A), did not. These results demonstrate that the delayed outward K + current and the negative slope resistance in steady-state I–V curve elicited by d-amphetamine may be responsible for the action potential bursts in central snail neurons elicited by d-amphetamine.

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