Potentiated response of corticotropin (ACTH) to repeated moderate hemorrhage requires amygdalar neuronal processing.

Abstract

We examined the role of the amygdala in the potentiation of the corticotropin (ACTH) response to a 10 mg/kg hemorrhage by a 1-hour episode of equivalent hypovolemia done 24 h earlier. Unanesthetized rats were studied on the fourth (D1) and fifth (D2) day after chronic implantation of arterial and venous catheters. Immunocytochemistry for Fos protein indicated that neurons in the central and medial nuclei of the caudal amygdala were activated by hemorrhage. We then tested the effect of excitotoxic destruction of the neurons in these areas by bilateral injections of ibotenic acid 10 days prior to catheter placement. In rats that were hemorrhaged on both D1 and D2, the responses of ACTH and corticosterone increased significantly from the first (H1) to the second hemorrhage (H2) in a control group injected with saline (p < 0.05) and in lesioned groups without bilateral damage of the Fos-responsive areas (p < 0.01). In the group with bilateral damage to these sites, the responses to H1 and H2 did not differ. Additional rats had H1 on D2 to control for the long-term effects of the chronic cannulation. The responses of ACTH to H1 on either D1 or D2 did not differ between the saline-injected controls and any of the lesioned groups. In contrast, the response of ACTH to H2 on D2 in rats with bilateral damage of the caudal amygdala was not significant and was less than the response of ACTH to H2 in both rats with unilateral damage of this area (p < 0.05) and those injected with saline (p < 0.05). We conclude that bilateral neuronal processing within the caudal amygdala is required for the potentiation of the response of ACTH to H2 by H1.