Forskolin reduces a transient potassium current in lobster neurons by a cAMP-independent mechanism

Abstract

Forskolin decreases the transient potassium current, I A, in voltage-clamped somata of identified neurons in the stomatogastric ganglion of the spiny lobster, Panulirus interruptus. The diterpene reduces the peak outward current and accelerates the rate of inactivation of I A. Forskolin has no detectable effects on two other identifiable potassium currents in these cells, I K(CA) and I K(V). Three identified stomatogastric neuron types (PD, PY, AB) have marked amounts of I A which are affected by forskolin; three other cell types (LP, IC, VD) have little or no I A, and forskolin has no effect on their outward currents. Bath application of 8-bromo-cAMP, N,N-dibutyryl-cAMP and IBMX do not affect I A. In addition, the forskolin analog, 1,9-dideoxyforskolin, which does not activate adenylate cyclase, mimics forskolin's effects on I A. Thus, the effects of forskolin on I A are not mediated by cAMP elevation.