IBOTENIC ACID LESIONS IN THE BED NUCLEUS OF THE STRIA TERMINALIS ATTENUATE CONDITIONED STRESS-INDUCED INCREASES IN PROLACTIN, ACTH AND CORTICOSTERONE

Citation
Ts. Gray et al., IBOTENIC ACID LESIONS IN THE BED NUCLEUS OF THE STRIA TERMINALIS ATTENUATE CONDITIONED STRESS-INDUCED INCREASES IN PROLACTIN, ACTH AND CORTICOSTERONE, Neuroendocrinology, 57(3), 1993, pp. 517-524
Citations number
48
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00283835
Volume
57
Issue
3
Year of publication
1993
Pages
517 - 524
Database
ISI
SICI code
0028-3835(1993)57:3<517:IALITB>2.0.ZU;2-X
Abstract
The contribution of the bed nucleus of the stria terminalis (BST) to t he expression of stress-induced increases in ACTH/corticosterone, prol actin and renin secretion was assessed. Neurons in the lateral part of the BST were destroyed with bilateral injections of the cell-selectiv e neurotoxin ibotenic acid (1.5 mug in 0.1 mul of solution per side). Two weeks later, the rats were stressed using an immobilization or con ditioned stress paradigm. Rats with lesions in the lateral part of the BST showed attenuated ACTH and corticosterone responses to conditione d stress. Bilateral ablation of lateral BST significantly reduced the prolactin secretory response to conditioned stress. The same lesions h ad no effect upon plasma increases in renin that occur in response to conditioned stress. Also, destruction of neurons in the BST did not af fect immobilization-induced increases in ACTH, corticosterone, prolact in or renin. Previous studies have demonstrated that ibotenic acid les ions in the central amygdala reduce corticosterone and renin response to conditioned stress. Thus, both the BST and central amygdala are imp ortant for the adrenocortical response to conditioned stress. Neurons in the central nucleus of the amygdala are part of the circuitry that mediates renin responses to conditioned stress. Neurons in the BST are important for the full expression of prolactin responses to condition ed stress. The neuronal circuitry and stressor specificity in the medi ation of prolactin, renin and ACTH/corticosterone responses are discus sed.