The role of ionic currents on procaine-elicited action potential bursts was studied in an identifiable RP1 neuron of the African snail, Achatina fulica Ferussac, using the two-electrode voltage clamp method. The RP1 neuron generated spontaneous action potentials and bath application of procaine at 10 mM reversibly elicited action potential bursts in a concentration-dependent manner. Voltage clamp studies revealed that procaine at 10 mM decreased [1] the Ca(superscript 2+) current, [2] the Na(superscript +) current, [3] the delayed rectifying K(superscript +) current I(subscript KD), and [4] the fast-inactivating K(superscript +) current (I(subscript A)). Action potential bursts were not elicited by 4-aminopyridine (4-AP), an inhibitor of IA, whereas they were seen after application of tetraethylammonium chloride (TEA), a blocker of the I(subscript K(Ca)) and IKD currents, and tacrine, an inhibitor of I(subscript KD). Pretreatment with U73122, a phospholipase C inhibitor, blocked the action potential bursts elicited by procaine. U73122 did not affect the I(subscript KD) of the RP1 neuron; however, U73122 decreased the inhibitory effect of procaine on the I(subscript KD). Tacrine decreased the TEA-sensitive I(subscript KD) of RP1 neuron but did not significantly affect the I(subscript A). Tacrine also successfully induced action potential bursts in the RP1 neuron. It is concluded that the inhibition on the I(subscript KD) is responsible for the generation of action potential bursts in the central snail RP1 neuron. Further, phospholipase C activity is involved in the procaine-elicited I(subscript KD) inhibition and action potential bursts.
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