A positive change in energy balance modulates TrkB expression in the hypothalamus and nodose ganglia of rats

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dc.contributor.author Zeeni, Nadine
dc.contributor.author Chaumontet, Catherine
dc.contributor.author Moyse, Emmanuel
dc.contributor.author Fromentin, Gilles
dc.contributor.author Tardivel, Catherine
dc.contributor.author Tome, Daniel
dc.contributor.author Jean, Andre
dc.contributor.author Darcel, Nicolas
dc.date.accessioned 2016-04-07T08:03:04Z
dc.date.available 2016-04-07T08:03:04Z
dc.date.copyright 2009
dc.date.issued 2016-04-07
dc.identifier.issn 0006-8993 en_US
dc.identifier.uri http://hdl.handle.net/10725/3506
dc.description.abstract Brain-derived neurotrophic factor (BDNF) and its TrkB receptor play critical roles in the synaptic activity and plasticity of mature neurons and enhance adult neurogenesis. Furthermore, treatment with BDNF has been found to attenuate weight gain or even cause weight loss and appetite suppression in rats. The aim of this study was to look at the effect of nutrient intake on BDNF concentrations and cellular proliferation in the brain. Adult male Wistar rats were given one of three diets for 6 weeks: high-carbohydrate, high-fat or high-fat pair-fed diets. Rats were sacrificed at the end of the feeding period and BDNF concentrations in the dorsal vagal complex (DVC), hypothalamus and plasma were measured by ELISA on protein extracts of these samples. Cellular proliferation in the DVC was quantified by Ki-67 immunohistochemistry. Neither BDNF levels nor proliferation were modified by the diet. Secondly, using rats that received the same diets, real-time PCR was performed in the DVC, hypothalamus and nodose ganglia in order to compare TrkB receptor levels. The results showed significantly lower TrkB levels in the hypothalamus and nodose ganglia of fasted rats receiving the high-fat diet when compared to the other groups. These two complementary methodological approaches suggest that there is a relationship between long-term dietary intake and BDNF. More precisely, TrkB expression is more responsive to energy states than to diet composition. An increment in energy stores thus triggers decreased BDNF anorexigenic signaling at the receptor level in the hypothalamus and nodose ganglia, but not in the DVC. en_US
dc.language.iso en en_US
dc.title A positive change in energy balance modulates TrkB expression in the hypothalamus and nodose ganglia of rats en_US
dc.type Article en_US
dc.description.version Published en_US
dc.author.school SAS en_US
dc.author.idnumber 201000400 en_US
dc.author.woa N/A en_US
dc.author.department Natural Sciences en_US
dc.description.embargo N/A en_US
dc.relation.journal Brain Research en_US
dc.journal.volume 1289 en_US
dc.article.pages 49-55 en_US
dc.keywords Brain-derived neurotrophic factor en_US
dc.keywords TrkB receptor en_US
dc.keywords High-fat diet en_US
dc.keywords Neuronal plasticity en_US
dc.keywords Gut–brain axis en_US
dc.keywords Brain plasticity en_US
dc.identifier.doi http://dx.doi.org/10.1016/j.brainres.2009.06.076 en_US
dc.identifier.ctation Zeeni, N., Chaumontet, C., Moyse, E., Fromentin, G., Tardivel, C., Tome, D., ... & Darcel, N. (2009). A positive change in energy balance modulates TrkB expression in the hypothalamus and nodose ganglia of rats. Brain research, 1289, 49-55. en_US
dc.author.email nadine.zeeni@lau.edu.lb
dc.identifier.url http://www.sciencedirect.com/science/article/pii/S0006899309013183

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