The participation of the amygdaloid complexes in the stress-induced release of ACTH was studied in the adult male rat. Unilateral and/or bilateral radiofrequency lesions were placed in the amygdalae or their efferent pathways. Plasma corticosterone concentrations were measured after either a leg break, tourniquet, or ether stress. Unilateral amygdaloid lesions did not block the effect of a contralaterally-applied tourniquet or leg break. Bilateral paired amygdaloid lesions blocked the effect of the leg break but not of ether or tourniquet. Bilateral paired lesions between the lateral hypothalamic area and the amygdalae also blocked the effect of the leg break but not ether or tourniquet, whereas bilateral lesions in the anterior portion of the striae terminali did not block the leg-break effect. These data suggest that the amygdalae facilitate rather than directly transmit neurogenic stress-induced signals (leg break) but not signals from systemic stresses (ether). Furthermore, one amygdaloid complex appears to be sufficient for achieving this effect. The pathway from the amygdalae to the hypothalamus involved in the facilitatory effect is probably a direct medial projection to the hypothalamus.