Role of the Paraventricular Nucleus in TNB-Induced Anorexia

Abstract

Inflammatory Bowel Disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract, often associated with reduced food intake (anorexia) and weight loss. The anorexia manifest following gastrointestinal inflammation can only be expressed if appropriate signals are communicated from the inflamed segment to the brain. Yet, the nature of these signals, and the identity of the brain sites processing these anorexigenic signals, are unknown. The present experiment evaluates the contribution of the paraventricular nucleus (PVN), a brain site rich in corticotropin releasing factor (CRF) receptors and known to be involved in the control of food intake, in the anorexia associated with experimental colitis. Colitis was induced, by trinitrobenzenesulfonic acid (TNB) treatment, in animals in which the PVN was ablated or in rats with sham brain surgeries. Results indicated clearly that the expression of the anorexia following TNB treatment is fully expressed even in the absence of the PVN. This result indicates that the integrity of the PVN is not necessary for the reduction of eating associated with intestinal inflammation, thus suggesting that CRF is also not critical to colitis-induced anorexia. inflammatory bowel disease (IBD); feeding; anorexia; gut-brain communication; paraventricular nucleus (PVN); interleukin-1 (IL-l); corticotropin-releasing-factor (CRF); neuroimmunology