Induction of brain-derived neurotrophic factor by leptin in the ventromedial hypothalamus

Komori, Tadasuke; Morikawa, Yoshihiro; Nanjo, Kishio; Senba, Emiko

doi:10.1016/j.neuroscience.2005.12.066

Cited by 110 publications

(98 citation statements)

References 36 publications

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“…Moreover i.v. administration of leptin at a dose sufficient to activate downstream signaling in the hypothalamus lead to up-regulation of BDNF mRNA and protein levels in the VMH, specifically in the dorsomedial aspect (Komori et al, 2006). Taken together, these data suggest that BDNF may mediate the anorexigenic and weight-reducing effects of melanocortin and leptin signaling, and lead us to hypothesize that BDNF in the VMH may also contribute to the anorexigenic effects of PP.…”

Section: Introductionmentioning

confidence: 79%

Y4 receptors and pancreatic polypeptide regulate food intake via hypothalamic orexin and brain-derived neurotropic factor dependent pathways

et al. 2010

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Gut-derived peptides are known to regulate food intake by activating specific receptors in the brain, but the target nuclei and neurons influenced are largely unknown. Here we show that peripherally administered pancreatic polypeptide (PP) stimulates neurons in key nuclei of the hypothalamus critical for appetite and satiety regulation. In the lateral hypothalamic area (LHA), also known as the feeding center, neurons expressing the orexigenic neuropeptide orexin co-localize with the early neuronal activation marker c-Fos upon i.p. injection of PP into mice. In the ventromedial hypothalamus (VMH), also known as the satiety center, neurons activated by PP, as indicated by induction of c-Fos immunoreactivity, express the anorexigenic brain-derived neurotrophic factor (BDNF). Activation of neurons in the LHA and VMH in response to PP occurs via a Y4 receptor-dependent process as it is not seen in Y4 receptor knockout mice. We further demonstrate that in response to i.p. PP, orexin mRNA expression in the LHA is down-regulated, with Y4 receptors being critical for this effect as it is not seen in Y4 receptor knockout mice, whereas BDNF mRNA expression is up-regulated in the VMH in response to i.p. PP in the fasted, but not in the non-fasted state. Taken together these data suggest that PP can regulate food intake by suppressing orexigenic pathways by down-regulation of orexin and simultaneously increasing anorexigenic pathways by upregulating BDNF.

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Section: Introductionmentioning

confidence: 79%

Y4 receptors and pancreatic polypeptide regulate food intake via hypothalamic orexin and brain-derived neurotropic factor dependent pathways

et al. 2010

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“…In addition to modulating the expression of POMC and NPY and the activity of neurons containing them in the Arc (Mizuno et al, 1998;Sahu, 1998;Ahima et al, 1999;Elias et al, 1999), it facilitates rewiring of circuits in that hypothalamic region (Pinto et al, 2004). After considering BDNF's well established role in synaptic plasticity elsewhere in the brain (Korte et al, 1995;Carter et al, 2002) and the ability of leptin to induce its expression in the VMH (Komori et al, 2006), it is reasonable to speculate about its potential involvement with the remodeling of feeding circuits. Future research should focus on elucidating whether BDNF produced in the VMH contributes to these reported forms of hypothalamic plasticity.…”

Section: Targets and Mechanisms Of Action Of Vmh/dmh-derived Bdnfmentioning

confidence: 99%

“…Additionally, BDNF mRNA levels are reduced by fasting in the VMH and nucleus of the solitary tract Bariohay et al, 2005;Tran et al, 2006). BDNF expression in these regions is also regulated by the peripheral satiety factors leptin and cholecystokinin (Bariohay et al, 2005;Komori et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Selective Deletion ofBdnfin the Ventromedial and Dorsomedial Hypothalamus of Adult Mice Results in Hyperphagic Behavior and Obesity

Unger

Calderón²,

Bradley³

et al. 2007

J. Neurosci.

340

319

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Brain-derived neurotrophic factor (BDNF) and its receptor TrkB are expressed in several hypothalamic and hindbrain nuclei involved in regulating energy homeostasis, developmentally and in the adult animal. Their depletion during the fetal or early postnatal periods when developmental processes are still ongoing elicits hyperphagic behavior and obesity in mice. Whether BDNF is a chief element in appetite control in the mature brain remains controversial. The required sources of this neurotrophin are also unknown. We show that glucose administration rapidly induced BDNF mRNA expression, mediated by Bdnf promoter 1, and TrkB transcription in the ventromedial hypothalamus (VMH) of adult mice, consistent with a role of this pathway in satiety. Using viral-mediated selective knock-down of BDNF in the VMH and dorsomedial hypothalamus (DMH) of adult mice, we were able to elucidate the physiological relevance of BDNF in energy balance regulation. Site-specific mutants exhibited hyperphagic behavior and obesity but normal energy expenditure. Furthermore, intracerebroventricular administration of BDNF triggered an immediate neuronal response in multiple hypothalamic nuclei in wild-type mice, suggesting that its anorexigenic actions involve short-term mechanisms. Locomotor, aggressive, and depressive-like behaviors, all of which are associated with neural circuits involving the VMH, were not altered in VMH/DMH-specific BDNF mutants. These findings demonstrate that BDNF is an integral component of central mechanisms mediating satiety in the adult mouse and, moreover, that its synthesis in the VMH and/or DMH is required for the suppression of appetite.

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“…From this point of view, the analogy and the relationship with leptin, secreted by adipose tissue and targeting to hypothalamus, and BDNF, secreted by both adipose tissue and hypothalamus, is noticeable. In fact, leptin increases the BDNF mRNA expression in VMN, DMN and in other brain areas where BDNF is widely expressed (Komori et al, 2006). According to Pardridge et al (1994) in the rat the mature form of BDNF does not cross the blood-brain barrier, suggesting a paracrine/autocrine activity of this protein in scAT, although other studies reported that about 70% of the BDNF collected from the jugular vein of humans is of brain origin (Rasmussen et al, 2009).…”

mentioning

confidence: 99%

Expression of NGF, BDNF and their receptors in subcutaneous adipose tissue of lactating cows

Colitti

Loor

Stefanon

2015

Research in Veterinary Science

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Induction of brain-derived neurotrophic factor by leptin in the ventromedial hypothalamus

Cited by 110 publications

References 36 publications

Y4 receptors and pancreatic polypeptide regulate food intake via hypothalamic orexin and brain-derived neurotropic factor dependent pathways

Y4 receptors and pancreatic polypeptide regulate food intake via hypothalamic orexin and brain-derived neurotropic factor dependent pathways

Selective Deletion ofBdnfin the Ventromedial and Dorsomedial Hypothalamus of Adult Mice Results in Hyperphagic Behavior and Obesity

Expression of NGF, BDNF and their receptors in subcutaneous adipose tissue of lactating cows

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