Intrinsic GABAergic neurons in the rat central extended amygdala

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Abstract
The present study examined the distribution, morphology, and connections of gamma‐aminobutyric acid‐immunoreactive (GABA‐IR) neuros in the three principal components of the central extended amygdala: the central amygdaloid nucleus, the bed nucleus of the stria terminalis (BNST) and the sublenticular substantia innominata. In the central nucleus, large numbers of GABA‐IR neurons were identified in the lateral, lateral capsular, and ventral subdivisions, though in the medial subdivision, GABA‐IR neurons were only present at very caudal levels. Combined immunocytochemistry‐Golgi impregnation revealed that GABA‐IR neurons in the lateral central nucleus were medium‐sized spiny neurons that were morphologically similar to GABAergic neurons in the striatum. Injections of horseradish peroxidase into the bed nucleus of the stria terminalis labeled a major proportion of the GABA‐IR neurons in the central nucleus. In the bed nucleus, the majority of GABA‐IR neurons were located in the anterolateral subdivision, ventral part of the posterolateral subdivision and the parastrial subdivision. GABA‐IR neurons in the anterolateral bed nucleus were of the typical mediumsized spiny type. Injections of horseradish peroxidase into the central nucleus labeled a few GABA‐IR neurons in the posterior part of the anterolateral bed nucleus. GABA‐IR neurons were identified in the sublenticular substantia innominata and medial shell of the nucleus accumbens and contributed to the continuum of GABA‐IR extending from the central nucleus to the bed nucleus. Injections of horseradish peroxidase (HRP) into the central nucleus, but not the BNST, labeled a few GABA‐IR neurons in the substantia innominata. The data point to GABA‐IR neurons being a characteristic feature of the central extended amygdala and that GABA‐IR neurons participate in the long intrinsic connections linking the major components of this structure. Since lesions of the stria terminalis and basolateral amygdaloid nucleus failed to deplete GABA‐IR terminals in the central nucleus, the role of GABA in local and short intrinsic connections in the central extended amygdala is discussed. Further, physiological findings implicating the intrinsic GABAergic system of the central extended amygdala in the tonic inhibition of brainstem efferents are reviewed.

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