Neural Controls of Prostaglandin 2 Pyrogenic, Tachycardic, and Anorexic Actions Are Anatomically Distributed

This paper describes a novel perspective on the neural mediation of prostaglandin's effect on fever and anorexia, emphasizing a neuroanatomical distribution of targeted sites rather than a single “center.” Fever and anorexia are induced by immune system challenges. Because these responses are adaptive when short lasting but deleterious when prolonged, an understanding of the mediating neural circuitry is important. Prostaglandins (PGE) are a critical signaling element for these immune responses. Despite the widespread distribution of PGE receptors throughout the brain, research focuses on the hypothalamic preoptic area as the mediating site of PGE action. Paraventricular nucleus of the hypothalamus (PVH), parabrachial nucleus (PBN), and nucleus tractus solitarius (NTS) neurons also express PGE receptors and are activated during systemic pathogen infection. A role for these neurons in PGE-induced fever, tachycardia, and anorexia is unexplored and is the subject of this report. A range of PGE2 doses was microinjected into third or fourth ventricles (v), or directly into the dorsal PVH, lateral PBN, and medial NTS, and core and brown adipose tissue temperature, heart rate, locomotor activity, and food intake were measured in awake, behaving rats. PGE2 delivery to multiple brain sites (third or fourth v, PVH, or PBN) induced a short- latency (