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

Forskolin decreases the transient potassium current, IA, 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 IA. Forskolin has no detectable effects on two other identifiable potassium currents in these cells, IK(Ca) and IK(V). Three identified stomatogastric neuron types (PD, PY, AB) have marked amounts of IA which are affected by forskolin; three other cell types (LP, IC, VD) have little or no IA, and forskolin has no effect on their outward currents. Bath application of 8-bromo-cAMP, N,N-dibutyryl-cAMP and IBMX do not affect IA. In addition, the forskolin analog, 1,9-dideoxyforskolin, which does not activate adenylate cyclase, mimics forskolin's effects on IA. Thus, the effects of forskolin on IA are not mediated by cAMP elevation.