Pittman Quentin J, Chen Xihua, Mouihate Abdeslam, Martin Sheilagh
Neuroscience Research Group and Department of Physiology and Biophysics, Faculty of Medicine University of Calgary, Calgary, Alberta, Canada.
Department of Biology, Mount Saint Vincent University, Halifax, Canada.
Ann N Y Acad Sci. 1998 Sep 29;856:53-61. doi: 10.1111/j.1749-6632.1998.tb08312.x.
There is now good evidence that vasopressin (AVP) acts, in the male rat, as a neurotransmitter in the ventral septal area to reduce fever. In light of the well known sexual dimorphism in the AVP innervation of the brain, we asked if female rats would (a) display fevers different from those seen in male rats, (b) respond to AVP with antipyresis, (c) display evidence of endogenous AVP-induced antipyresis during fever, and (d) display altered fevers and AVP involvement as a function of hormonal status. Our experiments indicate that female rats display larger fevers to intracranial prostaglandin E2 (PGE2) but not to systemic lipopolysaccharide or interleukin-1 beta than do male rats. The larger fevers may be due, in part, to a lack of AVP-induced antipyresis, as an AVP antagonist elevates PGE2 fever in male but not in female rats and dialysates of the ventral septal area show increased AVP levels only in male rats during defervescence. Nonetheless, females respond to exogenous AVP with antipyresis. Throughout late pregnancy, parturition, and lactation, PGE2 fevers are reduced, but this appears to be due to a general suppression of autonomic output not involving enhanced AVP antipyresis. Fevers due to lipopolysaccharide and interleukin-1 beta are also suppressed at this time, and in some animals, fevers are dramatically suppressed at about the time of parturition. Our results indicate that female rats may utilize different strategies for antipyresis than do male rats and that hormonal status may influence both peripherally generated and centrally activated fevers.
