The central nucleus of the rat amygdala (CeA) contains many corticotropin releasing factor (CRF) immunoreactive neurons. Previous studies have demonstrated that these CRF neurons project to brain stem regions responsible for modulation of autonomic outflow. Calcitonin gene-related peptide (CGRP) terminals overlap the distribution of CRF cell bodies in the CeA. These CGRP terminals mainly originate from cell bodies that are located in the pontine parabrachial nucleus. The present study examined the possibility that CRF cell bodies are innervated by CGRP terminals. The results suggest that over 35% of the CRF neurons in the CeA are contacted by CGRP terminals as judged by the indiscernible distances between the terminals and cell bodies and or dendrites. In addition, a dual-labeled electron microscopic technique demonstrates that CGRP terminals form synaptic contacts with CRF cell bodies and dendrites. This suggests that CGRP neurons in the parabrachial nucleus can modulate the activity of CRF amygdaloid brain stem efferents. Previous studies have shown that CRF, when administered into the central nervous system, produces increases in heart rate, blood pressure, and plasma catecholamines. CGRP administration into the amygdala has been shown to have a similar effect on the autonomic nervous system. It is, therefore, possible that CGRP could exert these effects via an amygdaloid CRF pathway.