Abstract
Inhibitory circuits in the basolateral nuclear complex of the amygdala (BNC) critical for controlling the acquisition, expression, and extinction of emotional responses are mediated by GABAergic interneurons (INs). Studies in rodents have demonstrated that separate IN subpopulations, identified by their expression of calcium-binding proteins and neuropeptides, play discrete roles in the intrinsic circuitry of the BNC. Far less is known about IN subpopulations in primates. In order to fill in this gap in our understanding of primate INs, the present investigation used dual-labeling immunohistochemistry for IN markers to identify subpopulations expressing cholecystokinin (CCK), calbindin (CB), calretinin (CR), and somatostatin (SOM) in somata and axon terminals in the monkey BNC. In general, colocalization patterns seen in somata and axon terminals were similar. It was found that there was virtually no colocalization of CB and CR, the two calcium-binding proteins investigated. Three subtypes of CCK-immunoreactive (CCK+) INs were identified on the basis of their expression of CR or CB: (1) CCK+/CR+; (2) CCK+/CB+); and (3) CCK+/CR-/CB-. Almost no colocalization of CCK with SOM was observed, but there was extensive colocalization of SOM and CB. CCK+, CR+, and CCK+/CR+ double-labeled axon terminals were seen surrounding pyramidal cell somata in basket-like plexuses, as well as in the neuropil. CB+, SOM+, and CB+/SOM+ terminals did not form baskets, suggesting that these IN subpopulations are mainly dendrite-targeting neurons. In general, the IN subpopulations in the monkey are not dissimilar to those seen in rodents but, unlike rodents, CB+ INs in the monkey are not basket cells.