Bistable behavior of inhibitory neurons controlling impulse traffic through the amygdala: Role of a slowly deinactivating K+ current

The intercalated cell masses of the amygdala are clusters of GABAergic neur ons located strategically to influence behavioral responsiveness. Indeed, t hey receive glutamatergic sensory inputs from the basolateral amygdaloid co mplex and generate feedforward inhibition in neurons of the central amygdal a that mediate important components of fear responses. In the present study , using whole-cell recording methods in coronal slices of the guinea pig am ygdala, we show that the activity of intercalated neurons is a function of their recent firing history because they express an unusual voltage-depende nt K+ conductance (termed I-SD for slowly deinactivating). This conductance activates in the subthreshold regime, inactivates in response to suprathre shold depolarizations, and deinactivates very slowly upon return to rest. A s a result, after bouts of suprathreshold activity, these cells enter a sel f-sustaining state of heightened excitability associated with an increased input resistance and a membrane depolarization. In turn, these changes incr ease the likelihood that ongoing synaptic activity will trigger orthodromic action potentials. However, because each orthodromic spike "renews" the in activation of I-SD, intercalated cells can remain hyperexcitable for a long time and, via the central amygdaloid nucleus, exert a lasting influence on behavior.