Differential impact of predator or immobilization stressors on central corticotropin-releasing hormone and bombesin-like peptides in Fast and Slow seizing rat.

Lines of rats selectively bred for amygdala excitability, as reflected by kindling rates in response to electrical stimulation, also exhibit differences in tests of anxiety. Inasmuch as corticotropin-releasing hormone (CRH) and bombesin (BN) have been associated with anxiety, regional levels and release of these peptides, as well as plasma adrenocorticotropic hormone (ACTH) and corticosterone, were assessed in 'Slow' and 'Fast' seizing rats following predator exposure (ferret) or immobilization. Ferret exposure elicited a greater increase of plasma ACTH and corticosterone concentrations in the Slow than in the Fast rats. In contrast, immobilization provoked a greater rise of plasma ACTH levels in the Fast rats, paralleling the vigorous struggling observed in this line. In Slow rats, stressor exposure elicited increased levels of ir-BN at the anterior hypothalamus, and increased ir-CRH at the median eminence/arcuate nucleus (Me/Arc), paraventricular hypothalamic nucleus (PVN) and pituitary (Pit), whereas decreased levels of ir-BN were found at the nucleus tractus solitarius (NTS). Fast rats likewise showed decreased ir-BN at the NTS, but unlike the Slow rats, ir-CRH was reduced in the Me/Arc, PVN and Pit in response to both stressors. In vivo microdialysis experiments revealed that in response to ferret exposure, the Slow rats showed a greater CRH release at the central nucleus of the amygdala (CeA) as compared to Fast rats. However, immobilization elicited a more pronounced release of CRH in Fast than in Slow rats. Taken together, the results demonstrate that these two lines of rats show differential endocrinological and neurochemical response patterns to these stressors.