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Review
. 2011 May;300(5):R1053-69.
doi: 10.1152/ajpregu.00776.2010. Epub 2011 Feb 23.

The lighter side of BDNF

Emily E Noble  1 , Charles J Billington, Catherine M Kotz, ChuanFeng Wang
Affiliations
Review

The lighter side of BDNF

Emily E Noble et al. Am J Physiol Regul Integr Comp Physiol. 2011 May.

Abstract

Brain-derived neurotrophic factor (BDNF) mediates energy metabolism and feeding behavior. As a neurotrophin, BDNF promotes neuronal differentiation, survival during early development, adult neurogenesis, and neural plasticity; thus, there is the potential that BDNF could modify circuits important to eating behavior and energy expenditure. The possibility that "faulty" circuits could be remodeled by BDNF is an exciting concept for new therapies for obesity and eating disorders. In the hypothalamus, BDNF and its receptor, tropomyosin-related kinase B (TrkB), are extensively expressed in areas associated with feeding and metabolism. Hypothalamic BDNF and TrkB appear to inhibit food intake and increase energy expenditure, leading to negative energy balance. In the hippocampus, the involvement of BDNF in neural plasticity and neurogenesis is important to learning and memory, but less is known about how BDNF participates in energy homeostasis. We review current research about BDNF in specific brain locations related to energy balance, environmental, and behavioral influences on BDNF expression and the possibility that BDNF may influence energy homeostasis via its role in neurogenesis and neural plasticity.

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Figures

Fig. 1.
Fig. 1.
Brain-derived neurotrophic factor (BDNF) and the central regulation of energy metabolism. Leptin is secreted from adipose tissue and activates receptors of the anorexigenic proopiomelanocortin (POMC) neurons of the arcuate nucleus (Arc) and neurons of the ventromedial nucleus of the hypothalamus (VMN). POMC neurons project to the hypothalamic paraventricular nucleus (PVN) and VMN, where they secrete alpha-melanocyte-stimulating hormone (α-MSH), which binds to the melanocortin receptor (MC4R). MC4R activation in the VMN controls BDNF expression; however, arcuate POMC neurons project sparsely to the VMN, and it is currently unknown whether α-MSH coming from these projections affects BDNF expression (284). Both leptin and α-MSH induce the expression of BDNF in the VMN. BDNF activates the tropomyosin-related kinase B (TrkB) receptor in neurons of the VMN and PVN, with consequences for energy metabolism (boxes on the left). In PVN neurons, BDNF removes inhibitory GABAA receptor clusters, allowing for greater neuronal excitability. Neurons of the PVN express corticotropin-releasing hormone (CRH) and in the PVN, effects of BDNF are attenuated when the CRH receptor is blocked by a receptor antagonist, indicating that BDNF activates the CRH-urocortin-CRH-R2 pathway. BDNF is expressed in the dorsal vagal complex (DVC) (box on the right), where it regulates energy metabolism as a downstream effector of the MC4R. BDNF is also expressed in the ventral tegmental area (VTA), where it is possibly involved in hedonic aspects of feeding (center box). *In contrast to the rest of the figure, this sentence refers to what happens when BDNF is deleted in the VTA. [Inset figure adapted from Paxinos and Watson (206).]
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