HYPERPOLARIZATION-ACTIVATED CURRENTS IN NEURONS OF THE RAT BASOLATERAL AMYGDALA

1. A single microelectrode was used to obtain current-clamp or voltage-clamp recordings from two neuronal cell types (pyramidal and late-firing neurons) in the basolateral nucleus of the amygdala (BLA) in slices of the rat ventral forebrain. Conductances activated by hyperpolarizing voltage steps from a holding potential of -70 mV were identified and their sensitivity to muscarinic modulation was determined using bath superfusion of carbachol. 2. Unclamped pyramidal neurons exhibited anomalous rectification, seen as a slowly developing depolarizing sag in the electronic potential in response to a hyperpolarizing current pulse. 3. Stepping voltage-clamped pyramidal neurons to command potentials of between -70 and -100 mV activated a slowly developing inward current (I(slow)) that followed a single exponential time course. Larger hyperpolarizing voltage steps evoked a rapidly developing inward current (I(Fast)) that preceded the development of I(Slow). 4. The I(Slow) component reversed at a level positive to the -70 mV holding potential. Its rate of activation accelerated as the hyperpolarizing voltage step was made more negative. The threshold for activation of the conductance underlying I(Slow) was approximately -60 mV, with half-activation occurring at -90 mV. 5. Extracellular Cs+ (2mM) blocked I(Slow) and eliminated anomalous rectification in unclamped pyramidal neurons. The inhibition of I(Slow) by Cs+ was also associated with membrane hyperpolarization and reduction of the medium afterhyperpolarization. I(Slow) was unaffected by extracellular Ba2+ (100 muM). The properties of this current appeared similar to that of the mixed cationic H-current previously identified in other neurons. 6. In comparison with pyramidal cells, unclamped late-firing neurons displayed a lesser but more rapidly developing anomalous rectification in response to large hyperpolarizations from rest. In voltage clamp, hyperpolarizing steps to command potentials more negative than -100 mV elicited I(Fast). Late-firing neurons expressed little or no I(Slow). 7. The properties of I(Fast) were identical in both pyramidal and late-firing neurons. This current reversed at a potential negative to -70 mV. Its rate of current activation increased with the magnitude of the hyperpolarizing voltage step. This rate was approximately sevenfold faster than I(Slow) activation recorded at the same membrane potential. I(Fast) was blocked by 2 mM extracellular Cs+ and reduced by 100 muM extracellular Ba2+. The threshold for activation of the underlying conductance was approximately -85 mV, with half-activation occurring at -112 mV. The properties of I(Fast) were similar to those of the inward rectifier current previously identified in other central neurons. 8. Carbachol (40 muM) largely blocked I(Fast) without affecting its rate of activation. This action of carbachol was prevented by 1 muM atropine, indicating mediation by muscarinic receptor activation. Carbachol did not inhibit I(Slow). 9. In BLA pyramidal neurons, I(Slow) appears to contribute to production of the medium afterhyperpolarization and the setting of the normal resting potential level. The I(Fast) of late-firing neurons may aid in production of the afterhyperpolarization and inhibition of this current component may contribute to the increased level of excitability produced by cholinergic afferent stimulation.