Amygdaloid lesions: differential effect on conditioned stress and immobilization-induced increases in corticosterone and renin secretion

• Published in: Neuroendocrinology Vol. 54; no. 2; p. 89
• Main Authors: Van de Kar, L D, Piechowski, R A, Rittenhouse, P A, Gray, T S
• Format: Journal Article
• Language: English
• Published: Switzerland 01-08-1991
• Subjects: Amygdala - drug effects; Amygdala - physiology; Animals; Conditioning (Psychology); Corticosterone - secretion; Ibotenic Acid - pharmacology; Male; Rats; Rats, Inbred Strains; Renin - blood; Renin - secretion; Restraint, Physical; Stress, Physiological - physiopathology
• ISSN: 0028-3835
• DOI: 10.1159/000125856

The purpose of this study was to examine the contribution of the central nucleus of the amygdala to the expression of stress-induced increase in corticosterone and renin secretion. Neurons in the central amygdaloid nucleus of male rats were destroyed by bilateral injections of ibotenic acid, a neurotoxin that destroys cells but leaves fibers of passage intact. Two weeks later, the rats were subjected to immobilization for 20 min or to a conditioned stress (conditioned emotional response) procedure. Central amygdala lesions inhibited the increases in plasma corticosterone after exposure to both conditioned stress and immobilization. Lesions in the lateral amygdala had no effect on the corticosterone response to either stressor. Lesions in the central amygdala attenuated the renin response to conditioned stress but not to immobilization. In contrast, lateral amygdala lesions potentiated the renin response to immobilization but did not affect the renin response to conditioned stress. The results confirm previous studies that demonstrate the importance of the central amygdaloid nucleus in the expression of corticosterone to immobilization stress. In addition, the results show that neurons within the central amygdaloid nucleus are necessary for the full expression of conditioned stress-induced increase in corticosterone and renin secretion. The results are discussed with respect to the potential pathways that mediate stress-induced increases in corticosterone and renin secretion.