Acute ether stress differentially affects corticotropin-releasing factor and urocortin 1 in the Brattleboro rat

Arginine-vasopressin (AVP), corticotropin-releasing factor (CRF) and urocortin 1 (Ucn1) play a role in the stress response. The CRF-producing paraventricular nucleus of the hypothalamus (PVN), oval bed nucleus of the stria terminalis (BSTov) and central amygdala (CeA), and the Ucn1-expressing non-preganglionic Edinger-Westphal nucleus (npEW) all possess AVP receptors. We hypothesized that AVP is involved in the response of these four brain centers to acute physiological (ether) stress. To test this hypothesis, we studied AVP-deficient Brattleboro (BB) rats using quantitative immunocytochemistry. First, we showed that non-stressed wild-type (WT) and BB rats did not differ from each other in Fos contents, indicating similar (immediate early) gene expression activity, but that in BB rats CRF contents were lower in the PVN and higher in the CeA. Second, we found that stress induced Fos response in the PVN, CeA and npEW with strengths different for each center, but similar for BB and WT rats. Finally, no effects of stress on CRF and Ucn1 contents were seen in the WT rat brain, but in BB rats stress increased CRF contents in the PVN, and the CeA revealed more CRF in stressed BB than in WT rats. On the basis of these results we propose that during acute stress AVP interacts with, especially, the PVN and the CeA, to change their rates of biosynthesis and/or release of CRF.

Research highlights
► Effect of acute ether stress on Brattleboro rat, which lacks AVP.
► Fos activation in PVN, BSTov, CeA and npEW not affected by AVP.
► CRF in the PVN lower and in the CeA higher in Brattleboro rats.
► during acute stress AVP interacts with CRF in the PVN and the CeA.