Journal
BEHAVIOURAL BRAIN RESEARCH
Volume 363, Issue -, Pages 118-125Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbr.2019.01.042
Keywords
Anorexia; Hippocampus; Microglia; TNF-alpha; IL-6; IL-1 beta
Categories
Funding
- Programa de Apoyo a Proyectos de Investigacion e Innovacion Tecnologica (PAPIIT) from Universidad Nacional Autonoma de Mexico (UNAM) [IN202315, IN201913, IN201915, IN205718]
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Anorexia by osmotic dehydration is an adaptive response to hypernatremia and hyperosmolaemia induced by ingestion of a hypertonic solution. Dehydration-induced anorexia (DIA) reproduces weight loss and avoidance of food, despite its availability. By using this model, we previously showed increased reactive astrocyte density in the rat dorsal hippocampus, suggesting a pro-inflammatory environment where microglia may play an important role. However, whether such anorexic condition increases a pro-inflammatory response is unknown. The aim of this study was to test if DIA increases microglial density in the dorsal hippocampus, as well as the expression of pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6) and interleukin 1 beta (IL-1 beta) in the hippocampus of young female rats. Our results showed that DIA significantly increased microglial density in CA2-CA3 and dentate gyrus (DG) but not in CA1. However, forced food restriction (FFR) only increased microglial density in the DG. Accordingly, the activated/resting microglia ratio was significantly increased in CA2-CA3 and DG, in DIA and FFR groups. Finally, western blot analysis showed increased expression of IBA1, TNF-alpha, IL-6 and IL-1 beta in the hippocampus of both experimental groups. We conclude that anorexia triggers increased reactive microglial density and expression of TNF-alpha, IL-6 and IL-1 beta; this environment may result in hippocampal neuroinflammation.
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