Interleukin-1β (IL-1β), a cytokine with pronounced central effects such as fever, anorexia, analgesia, etc., is also known to activate the hypothalamo–pituitary–adrenal (HPA) axis. Corticotropin releasing hormone (CRH) neurons located in the hypothalamus are important for HPA activation. The cell bodies of CRH neurons are located in the paraventricular nucleus (PVN) and their terminals are present in the median eminence (ME). Although the catecholamines, norepinephrine (NE) and dopamine (DA) are believed to be crucial factors in the stimulation of CRH neurons, it is not clear if they affect the cell bodies or terminals of these neurons to cause HPA activation. This study was done to determine if IL-1β affects NE and DA release at the level of CRH cell bodies or their terminals. Adult male Sprague–Dawley rats were implanted with two push–pull cannulae, one in the PVN and another in the ME, and were subjected to push–pull perfusion. They were treated either with 0, 1 or 5μg of IL-1β. Perfusates were collected for 2h after treatment and analyzed for NE concentrations using HPLC-EC. NE levels in the control and low dose groups did not change significantly during the entire period of observation both in the PVN and ME. In contrast, treatment with 5μg of IL-1β produced a marked increase in NE release in the PVN at 20 and 40min post-treatment. NE release in the ME increased from 10 to 140min post-treatment. There were no significant changes in the release of DA from both these areas. These results indicate that IL-1β increases NE levels both in the PVN and in the ME and this could be a possible mechanism by which it stimulates the HPA axis.