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Neuroscience Research Group, University of Calgary, Alberta, Canada.

1. Arg8-vasopressin (AVP)-containing neurones of the bed nucleus of the stria terminalis (BST), which terminate in the ventral septal area (VSA) of the rat brain, provide a pathway which controls body temperature during fever. The present study was conducted to test the hypothesis that interleukin-1 beta (IL-1 beta) may trigger the antipyretic response by evoking AVP release from BST neurones projecting into the VSA. 2. The push-pull perfusion technique and radioimmunoassay were utilized to determine the AVP concentrations of retrieved VSA perfusion fluid in urethane-anaesthetized rats following BST infusion of vehicle or IL-1 beta (125 or 500 pg (2 microliters)-1). 3. Ventral septal AVP levels significantly increased from basal levels, in a dose-related manner, in response to IL-1 beta (0-500 pg). Electrical stimulation of the same areas of the BST also evoked AVP release into the VSA. 4. IL-1 beta infusions and electrical stimulation of the BST resulted in significant increases in rectal temperature. In IL-1 beta-treated animals (500 pg), the change in body temperature and VSA AVP release were negatively correlated (P < 0.001). However, external heating of the animals to approximately the same levels as electrically stimulated or IL-1 beta treated rats did not affect basal AVP release. 5. These data show that IL-1 beta is a potent stimulus for AVP release from BST neurones and supports BST involvement in neuro-immune interactions. We propose, that in addition to febrogenesis, IL-1 beta is also a key component in the process of endogenous antipyresis by activating vasopressinergic BST neurones to release AVP during fever.

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