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The ionic mechanism of the effect of intracellularly injected adenosine 3',5'-cyclic monophosphate (cAMP) on the membrane of identified neuron L5 of Aplysia kurodai was investigated with conventional voltage-clamp and ion-substitution techniques. The intracellular elevation of cAMP caused an inward current (IcAMP), which was not accompanied by a significant change in membrane conductance at potentials more hyperpolarized than -60 mV. The current increased over the voltage range (-50 to -30 mV) associated with a conductance decrease and decreased at potentials more hyperpolarized than -60 mV. Elevated intracellular cAMP was found to enhance a region of negative slope resistance in steady-state I-V relations. Duration of the IcAMP was greatly prolonged by bath-applied isobutylmethylxanthine (50 microM), but imidazole (10 mM) had an opposite effect on the IcAMP. Tolbutamide (5 mM), a protein kinase inhibitor, reduced the IcAMP. The current was not affected by the presence of bath-applied TTX (50 microM), ouabain (50 microM), or triaminopyrimidine (5 mM). Reduction of [Na+]0 reversibly decreased the IcAMP. Li+ could largely substitute for Na+. Alterations of [K+]0, and bath application of 4-AP (5 mM) and TEA (30 mM) did not affect the IcAMP. In the presence of Na+, Cl-, and divalent cations such as Ca2+ and Ba2+ inhibited the IcAMP. These results suggest that fast elevation of intracellular cAMP induces a TTX-resistant slow Na+ inward current, and the current might be due to activation of cAMP-dependent protein kinase.

Influences of pressure-injected cyclic AMP on the membrane current and characteristics of an identified neuron of Aplysia kurodai.