The possible functional roles of the transient K+ current, IA, in basolateral amygdala (BLA) neurons were studied using a rat brain slice preparation and conventional intracellular recording techniques. Conditioning depolarization, which inactivates IA, slowed the action potential repolarization while conditioning hyperpolarization accelerated the action potential repolarization. 4-Aminopyridine (4-AP, 100 microM), a specific IA antagonist, also caused a clear delay in spike repolarization similar to the effect of conditioning depolarization suggesting that IA is involved in the action potential repolarization. When BLA neurons were excited by injecting long depolarizing current pulses (500 ms), they responded with an initial rapid discharge of action potentials which slowed or accommodated; an afterhyperpolarization (AHP) followed the depolarizing current pulses. Superfusion of 4-AP (100 microM) blocked accommodation resulting in an increase in action potential discharge in 74% (32 out of 43) neurons tested. The remaining 11 cells responded with an increased frequency of discharge of the first few action potentials. Unlike the effect of cadmium (Cd2+, 100 microM), a calcium channel blocker, 4-AP did not reduce the AHP. In the presence of norepinephrine (NE, 10 microM), a neurotransmitter which has been shown to block calcium-activated potassium conductance, 4-AP caused a further increase in the number and frequency of action potential discharge. In addition, in BLA neurons, spontaneous interictal and ictal-like events were observed at low and high concentrations of 4-AP, respectively. We conclude that IA is involved in the action potential repolarization as well as spike frequency adaptation in BLA neurons and that these actions may contribute to the convulsant effect of 4-AP.