The primate amygdaloid complex is a prominent structure in the medial temporal lobe that comprises a variety of cytoarchitectonically distinct nuclei and cortical regions. The present study employed immunohistochemical and in situ hybridization techniques to determine the distribution of GABAergic cells, fibers, and terminals in the macaque monkey amygdala. Using a monoclonal antibody to GABA, immunoreactive neurons were observed throughout the amygdaloid complex (constituting approximately 20% of the neurons in the lateral nucleus), with higher densities located in the intercalated nuclei, amygdalohippocampal area, and posterior cortical nucleus. The lowest densities of labeled cells were observed in the central and medial nuclei. Interestingly, despite the low number of GABA-immunoreactive neurons, the terminal density in the central nucleus was among the highest in the amygdala. The GABAergic neurons in the amygdala were heterogeneous in morphology, and three general classes of immunopositive aspiny cells were observed. Using mRNA probes for glutamic acid decarboxylase (GAD: GAD65 and GAD67), in situ hybridization demonstrated distributions of labeled cells that generally replicated the immunohistochemical findings. One exception was in the central nucleus where, in contrast to the low number of immunohistochemically labeled cells, both GAD probes labeled large numbers of neurons. These studies on the organization of GABAergic circuits in the primate amygdala are significant because alterations of function in the human amygdala have been implicated in the pathogenesis of temporal lobe epilepsy and in the etiology of affective and other behavioral disorders. The present study provides baseline information with which to evaluate the role of GABAergic systems in amygdala-mediated behaviors and the potential contribution of GABAergic dysfunction in amygdala-associated disorders.
Pitkänen et al. (Fri,) studied this question.