Journal of Neuroscience, Vol 14, 2200-2224, Copyright © 1994 by Society for Neuroscience
The distribution of GABAergic cells, fibers, and terminals in the monkey amygdaloid complex: an immunohistochemical and in situ hybridization study
A Pitkanen and DG Amaral
University of Kuopio, Department of Neurology, Finland.
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.
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