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

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.