Neural plasticity, neuropeptides and anxiety in animals--implications for understanding and treating affective disorder following traumatic stress in humans.

Exposure of rats to cats (predator stress) lastingly increases rodent anxiety-like behavior (ALB) in the elevated plus-maze. Previous work shows that lasting changes in ALB following predator stress depend on NMDA and CCKB receptors. In this paper we describe the effects of differing degrees of predator exposure on behavior. Effects depend on the behavioral measure. In general, exposure to predator odor is less provocative of lasting change in ALB than is unprotected exposure to a cat. In addition, we examine the development of effects of unprotected predator exposure over time. Lasting effects on ALB begin at 30 min to 1 h after predator stress and persist for at least 3 weeks. We also report a complex pattern of effects of predator stress on neuroendocrine and stress peptide (bombesin, CRF and AVP) levels in a variety of brain areas. Not surprisingly, predator exposure increases plasma levels of corticosterone and ACTH. Central changes in peptide content in the hypothalamo-pituitary axis, related hypothalamic nuclei, limbic and brain stem areas are also noted. Finally, path analysis demonstrates a replicable relationship between cat behavior, rat defensive behavior and degree of increase in ALB one week later. It is proposed that behavioral changes following predator stress may model anxiety associated with PTSD.