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Brain-Derived Neurotrophic Factor Plays a Role as an Anorexigenic Factor in the Dorsal Vagal Complex

Laboratoire de Physiologie Neurovégétative, Unité Mixte de Recherche Université Paul Cézanne Aix-Marseille III, Centre National de la Recherche Scientifique (Unité Mixte de Recherche 6153), Institut National de la Recherche Agronomique (Unité Mixte de Recherche 1147), Faculté des Sciences et Techniques, 13397 Marseille cedex 20, France

Address all correspondence and requests for reprints to: Bruno Lebrun, (MCF), Laboratoire de Physiologie Neurovégétative, Unité Mixte de Recherche Université Paul Cézanne Aix-Marseille III, Centre National de la Recherche Scientifique (Unité Mixte de Recherche 6153), Institut National de la Recherche Agronomique (Unité Mixte de Recherche 1147), Faculté des Sciences et Techniques, BP 351, 13397 Marseille cedex 20, France. E-mail: bruno.lebrun{at}univ.u-3mrs.fr.

Brain-derived neurotrophic factor (BDNF) has recently been implicated as an anorexigenic factor in the central control of food intake. Previous studies focused on the hypothalamus as a probable site of action for this neurotrophin. It was demonstrated that BDNF is an important downstream effector of melanocortin signaling in the ventromedial hypothalamus. In this study, we addressed whether BDNF can modulate food intake in the hindbrain autonomic integrator of food intake regulation, i.e. the dorsal vagal complex (DVC). To this end, we used two complementary methodological approaches in adult rats. First, we measured the effects of intraparenchymal infusions of exogenous BDNF within the DVC on food intake and body weight. Second, we measured the endogenous BDNF protein content in the DVC and hypothalamus after food deprivation, refeeding, or peripheral treatments by the anorexigenic hormones leptin and cholecystokinin (CCK). BDNF infusion within the DVC induced anorexia and weight loss. In the DVC, BDNF protein content decreased after 48 h food deprivation and increased after refeeding. Acute and repetitive peripheral leptin injections induced an increase of the BDNF protein content within the DVC. Moreover, peripheral CCK treatment induced a transient increase of BDNF protein content first in the DVC (30 min after CCK) and later on in the hypothalamus (2 h after CCK). Taken together, these results strongly support the view that BDNF plays a role as an anorexigenic factor in the DVC. Our data also suggest that BDNF may constitute a common downstream effector of leptin and CCK, possibly involved in their synergistic action.

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