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The intercalated cell masses of the amygdala are clusters of GABAergic neurons located strategically to influence behavioral responsiveness. Indeed, they receive glutamatergic sensory inputs from the basolateral amygdaloid complex and generate feedforward inhibition in neurons of the central amygdala that mediate important components of fear responses. In the present study, using whole-cell recording methods in coronal slices of the guinea pig amygdala, we show that the activity of intercalated neurons is a function of their recent firing history because they express an unusual voltage-dependent K+ conductance (termedISD for slowly deinactivating). This conductance activates in the subthreshold regime, inactivates in response to suprathreshold depolarizations, and deinactivates very slowly upon return to rest. As a result, after bouts of suprathreshold activity, these cells enter a self-sustaining state of heightened excitability associated with an increased input resistance and a membrane depolarization. In turn, these changes increase the likelihood that ongoing synaptic activity will trigger orthodromic action potentials. However, because each orthodromic spike “renews” the inactivation of ISD, intercalated cells can remain hyperexcitable for a long time and, via the central amygdaloid nucleus, exert a lasting influence on behavior.

Bistable Behavior of Inhibitory Neurons Controlling Impulse Traffic through the Amygdala: Role of a Slowly Deinactivating K+Current

Bistable Behavior of Inhibitory Neurons Controlling Impulse Traffic through the Amygdala: Role of a Slowly Deinactivating K⁺Current