Search

The role of catecholamines in regulating the neuroendocrine stress response is controversial. We have investigated the effects of unilateral ventral noradrenergic bundle (VNAB) lesions on corticotrophin-releasing factor (CRF) and proenkephalin A mRNA responses in the parvocellular paraventricular nucleus (pPVN) to both physical and psychological stresses. We have also determined the effects of direct bilateral PVN lesions on CRF mRNA, plasma ACTH and corticosterone responses to psychological stress. 6-OHDA lesions whether to the VNAB or direct to the PVN did not result in any change in basal levels of CRF mRNA. Depletion of endogenous noradrenaline following unilateral lesions of the VNAB did not affect the CRF mRNA or the proenkephalin A mRNA response to stress. These data suggest that noradrenergic pathways are not involved in maintaining basal levels of CRF mRNA and that the noradrenergic input through the VNAB does not mediate the accumulation of CRF and proenkephalin A mRNAs in response to these stressors. Direct bilateral lesions to the PVN prevented the accumulation of CRF mRNA but not the ACTH and corticosterone responses to restraint stress. This suggests that monoamines are involved in the regulation of CRF mRNA through a mechanism independent of CRF-41 secretion.

It is generally assumed that the stress response of different strains of rat will be identical following exposure to acute stress. In the present study we have examined the activation of the hypothalamo-pituitary-adrenal axis in the Wistar, Sprague-Dawley and CFY strains of rat following exposure to either the predominantly psychological stress of restraint or the physical stress of i.p. hypertonic saline injection. We have investigated the hypothalamic activation of corticotrophin-releasing factor (CRF) and proenkephalin A (PEA) mRNAs in the parvocellular cells of the paraventricular nucleus (PVN) and arginine vasopressin (AVP) in both the magnocellular and parvocellular regions in the PVN following acute stress. In addition we have measured corticosterone as an index of end-point activation. Circulating corticosterone and CRF mRNA were increased in all three strains following either stress. AVP and PEA mRNAs were increased following hypertonic saline but only in the CFY strain following restraint. Overall the relative increase in the parameters measured was greater in the CFY strain of rat than the other strains. These data demonstrate marked differences in response to acute stress in the three strains of rat examined. These varying responses must be taken into consideration when designing or interpreting any study investigating the stress response.