CENTRAL INTERLEUKIN-1-BETA STIMULATION OF VASOPRESSIN RELEASE INTO THE RAT-BRAIN - ACTIVATION OF AN ANTIPYRETIC PATHWAY

1. Arg(8)-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 tempera ture during fever. The present study was conducted to test the hypothe sis that interleukin-1 beta (IL-1 beta) may trigger the antipyretic re sponse by evoking AVP release from BST neurones projecting into the VS A. 2. The push-pull perfusion technique and radioimmunoassay were util ized to determine the AVP concentrations of retrieved VSA perfusion fl uid in urethane-anaesthetized rats following BST infusion of vehicle o r IL-1 beta (125 or 500 pg (2 mu l)(-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 sam e areas of the BST also evoked AVP release into the VSA. 4. IL-1 beta infusions and electrical stimulation of the BST resulted in significan t increases in rectal temperature. In IL-1 beta-treated animals (500 p g), the change in body temperature and VSA AVP release were negatively correlated (P<0.001). However, external heating of the animals to app roximately the same levels as electrically stimulated or 5. IL-1 beta- treated rats did not affect basal AVP release. These data show that IL -1 beta is a potent stimulus for AVP release from BST neurones and sup ports BST involvement in neuro-immune interactions. We propose, that i n addition to febrogenesis, IL-1 beta is also a key component in the p rocess of endogenous antipyresis by activating vasopressinergic BST ne urones to release AVP during fever.