Contextual inhibitory gating of impulse traffic in the intra-amygdaloid network.

New data on the organization of the intra-amygdaloid circuit is reviewed, beginning with the basolateral (BL) complex, the main input station of the amygdala for sensory afferents, and concluding with the central (CE) nucleus, an important source of projections to brain-stem structures mediating fear responses. The BL complex is endowed with a highly divergent system of intrinsic glutamatergic connections. Yet, BL projection cells have unusually low firing rates. This apparent contradiction is explained by the presence of powerful inhibitory pressures in the BL amygdala: (1) interneurons that generate large-amplitude inhibitory synaptic potentials and (2) projection cells that express a Ca(2+)-dependent K(+) current that can be activated by subthreshold synaptic inputs. Likewise, excitatory projections from the BL amygdala to the CE nucleus are controlled by clusters of GABAergic neurons, termed the intercalated (ITC) cell masses. In response to BL inputs, ITC cells generate feedforward inhibition in CE neurons. However, ITC neurons exhibit properties that allow them to modify the amount of inhibition they generate depending on the distribution of BL activity in space and time. Indeed, ITC cell masses can inhibit each other via lateromedial connections. Moreover, they express an unusual K(+) conductance that modifies their response to BL inputs depending on their recent firing history. Thus, inhibitory mechanisms of the amygdala allow for flexible, context-dependent gating of BL impulses to the CE nucleus.