Ibotenic acid lesions in the bed nucleus of the stria terminalis attenuate conditioned stress-induced increases in prolactin, ACTH and corticosterone.

The contribution of the bed nucleus of the stria terminalis (BST) to the expression of stress-induced increases in ACTH/corticosterone, prolactin and renin secretion was assessed. Neurons in the lateral part of the BST were destroyed with bilateral injections of the cell-selective neurotoxin ibotenic acid (1.5 micrograms in 0.1 microliter of solution per side). Two weeks later, the rats were stressed using an immobilization or conditioned stress paradigm. Rats with lesions in the lateral part of the BST showed attenuated ACTH and corticosterone responses to conditioned stress. Bilateral ablation of lateral BST significantly reduced the prolactin secretory response to conditioned stress. The same lesions had no effect upon plasma increases in renin that occur in response to conditioned stress. Also, destruction of neurons in the BST did not affect immobilization-induced increases in ACTH, corticosterone, prolactin or renin. Previous studies have demonstrated that ibotenic acid lesions in the central amygdala reduce corticosterone and renin response to conditioned stress. Thus, both the BST and central amygdala are important 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 conditioned stress. The neuronal circuitry and stressor specificity in the mediation of prolactin, renin and ACTH/corticosterone responses are discussed.