We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
L-arginine abolishes the hypothalamic serotonergic activation induced by central interleukin-1β administration to normal rats.
- Authors
Iuras, Anderson; Telles, Mônica M.; Andrade, Iracema S.; Santos, Gianni M. S.; Oyama, Lila M.; Nascimento, Cláudia M. O.; Silveira, Vera L. F.; Ribeiro, Eliane B.
- Abstract
IL-1β-induced anorexia may depend on interactions of the cytokine with neuropeptides and neurotransmitters of the central nervous system; control of energy balance and serotonin is likely to be one catabolic mediator targeted by IL-1β. In the complex interplay involved in feeding modulation, nitric oxide has been ascribed a stimulatory action, which could be of significance in counteracting IL-1β effects. The present study aims to explore the participation of the nitric oxide and the serotonin systems on the central mechanisms induced by IL-1β and the relevance of their putative interactions to IL-1β hypophagia in normal rats. Serotonin levels were determined in microdialysates of the ventromedial hypothalamus after a single intracerebroventricular injection of 10 ng of IL-1β , with or without the pre-injection of 20 μg of the nitric oxide precursor L-arginine. IL-1β significantly stimulated hypothalamic serotonin extracellular levels, with a peak variation of 130 ±37% above baseline. IL- 1β also reduced the 4-h and the 24-h food intakes (by 23% and 58%, respectively). The IL-1β- induced serotonergic activation was abolished by the pre-injection of L-arginine while the hypophagic effect was unaffected. The data showed that one central effect of IL-1β is serotonergic stimulation in the ventromedial hypothalamus, an action inhibited by nitric oxide activity. It is suggested that, although serotonin participates in IL-1β anorexia, other mechanisms recruited by IL-1β in normal rats are able to override the absence of the serotonergic hypophagic influence.
- Subjects
INTERLEUKIN-1; APPETITE loss; NEUROTRANSMITTERS; CENTRAL nervous system; LIMBIC system
- Publication
Journal of Neuroinflammation, 2013, Vol 10, Issue 1, p1
- ISSN
1742-2094
- Publication type
Article
- DOI
10.1186/1742-2094-10-147