Direct Projections from the Central Amygdaloid Nucleus to the Hypothalamic Paraventricular Nucleus: Possible Role in Stress-Induced Adrenocorticotropin Release

Abstract

The amygdala, particularly the central amygdaloid nucleus, is important for the expression of adrenocorticotropin and corticosterone responses during stress. The aim of the present study was to determine if the central amygdaloid nucleus directly innervated the hypothalamic paraventricular nucleus. To accomplish this aim, the Phaseolus vulgaris leucoagglutinin lectin anterograde tracing method was used. Injections of the tracer into the medial central amygdaloid nucleus resulted in axonal and terminal labeling within the medial and lateral parvocellular parts of the caudal paraventricular nucleus. A dense patch of labeling was observed within the lateral wing of the lateral part of the parvocellular paraventricular nucleus. Only a few labeled axons were observed within the paraventricular nucleus of animals that had lectin injections localized to the lateral part of the central nucleus. Tracer injections localized to the medial amygdaloid nucleus resulted in axonal and terminal labeling primarily within the anterior parvocellular and periventricular regions of the paraventricular hypothalamic nucleus. Sparse to moderate axonal and terminal labeling was observed within the magnocellular parts of the paraventricular nucleus in animals that had injections of tracer into either the medial central nucleus or the medial nucleus. No labeling was observed within the paraventricular nucleus of animals that had injections of lectin within other amygdaloid nuclei or adjacent regions of the striatum. The results demonstrated a topographically organized projection from the amygdala to the hypothalamic paraventricular nucleus. The central nucleus mainly innervates the caudal lateral and medial parvocellular paraventricular nucleus. The medial nucleus innervates the rostral parvocellular parts of the paraventricular nucleus. These pathways could form the anatomical substrates of amygdaloid modulation of neuroendocrine responses to stressors.