Behavioral and physiological studies have implicated the central nucleus of the amygdala (CNA) in the motoric (both somatic and visceral) expression of fear behavior. Anatomically, the CNA is well situated to modulate information concerning the external and internal environment, via limbic cortices, amygdala and hypothalamus, and to affect autonomic and somatc behavior via projections to the basal forebrain, ventral mid-brain and brain stem. The distribution pattern of cortical afferent termination in the CNA is poorly understood though the available evidence indicates that these afferents terminate in specific cytoarchitectonic zones. This may reflect specific interactions with efferent projection neuron populations in the CNA that likewise show highly specific distributions. Moreover, terminals containing met-enkephalin and pro-opiomelanocortin (POMC) derived peptides are distributed over specific parts of the CNA. Preliminary studies suggest that these distribution patterns are congruent with both the distribution of certain cortical afferents and with specific populations of projection neurons. The proposed investigations are designed to test the applicant's hypotheses that (a) cortical afferents that show nonoverlapping distributions in the CNA innervate different populations of projection neurons and (b) that met-enkephalin and POMC peptides interact with cortical afferents contacting similar projection neurons. Results may lead to a better understanding of how the CNA processes cortical information and how endogenous peptides (and drugs that mimic/block these peptides) influence behavior. The distribution of cortical afferents in the CNA will be determined using the anterograde transport of peroxidase conjugated lectins. Data will be correlated with the applicant's previous work on the distributions of projection neurons in the CNA. Evidence of direct cortical innervation of CNA projection neurons and interactions with terminals containing met-enkephalin and POMC peptides will be sought at the ultrastructural level using combined lesion-induced degeneration of cortical afferents, peptide immunocytochemistry and retrograde transport of horseradish peroxidase from focal injections into the medulla and basal forebrain.
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