scholarly journals Brain‐derived neurotrophic factor exerts depolarizing effects on hypothalamic paraventricular nucleus neurons (1126.6)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
William McIsaac ◽  
Alastair Ferguson
Keyword(s):  
Paraventricular Nucleus ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Hypothalamic Paraventricular Nucleus

Brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus reduces energy intake

2007 ◽  
Vol 293 (3) ◽  
pp. R1003-R1012 ◽  
Author(s):  
ChuanFeng Wang ◽  
Eric Bomberg ◽  
Charles Billington ◽  
Allen Levine ◽  
Catherine M. Kotz
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Paraventricular Nucleus ◽  
Neurotrophic Factor ◽  
Body Weight Gain ◽  
Brain Derived Neurotrophic Factor ◽  
Brain Regions ◽  
Hypothalamic Paraventricular Nucleus ◽  
Bdnf Mrna ◽  
Hypothalamic Arcuate Nucleus

Recent studies show that brain-derived neurotrophic factor (BDNF) decreases feeding and body weight after peripheral and ventricular administration. BDNF mRNA and protein, and its receptor tyrosine kinase B (TrkB) are widely distributed in the hypothalamus and other brain regions. However, there are few reports on specific brain sites of actions for BDNF. We evaluated the effect of BDNF in the hypothalamic paraventricular nucleus (PVN) on feeding. BDNF injected unilaterally or bilaterally into the PVN of food-deprived and nondeprived rats significantly decreased feeding and body weight gain within the 0- to 24-h and 24- to 48-h postinjection intervals. Effective doses producing inhibition of feeding behavior did not establish a conditioned taste aversion. PVN BDNF significantly decreased PVN neuropeptide Y (NPY)-induced feeding at 1, 2, and 4 h following injection. BDNF administration in the PVN abolished food-restriction-induced NPY gene expression in the hypothalamic arcuate nucleus. In conclusion, BDNF in the PVN significantly decreases food intake and body weight gain, suggesting that the PVN is an important site of action for BDNF in its effects on energy metabolism. Furthermore, BDNF appears to interact with NPY in its anorectic actions, although a direct effect on NPY remains to be established.

scholarly journals Chronic administration of brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus reverses obesity induced by high-fat diet

2010 ◽  
Vol 298 (5) ◽  
pp. R1320-R1332 ◽  
Author(s):  
ChuanFeng Wang ◽  
Rebecca J. Godar ◽  
Charles J. Billington ◽  
Catherine M. Kotz
Keyword(s):  
Body Weight ◽  
Body Fat ◽  
Paraventricular Nucleus ◽  
Neurotrophic Factor ◽  
High Fat Diet ◽  
Control Diet ◽  
Brain Derived Neurotrophic Factor ◽  
Hypothalamic Paraventricular Nucleus ◽  
High Fat ◽  
Metabolic Indices

An acute injection of brain-derived neurotrophic factor (BDNF) in the hypothalamic paraventricular nucleus (PVN) reduces body weight by decreasing feeding and increasing energy expenditure (EE), in animals on standard laboratory chow. Animals have divergent responses to a high-fat diet (HFD) exposure, with some developing obesity and others remaining lean. In the current study, we tested two hypotheses: 1) BDNF in the PVN reverses HFD-induced obesity, and 2) animals with higher body fat have a greater physiological response to BDNF than those with less body fat. Eighty-four 10-wk old rats were allowed HFD ad libitum for 9 wk and then prepared with bilateral PVN cannulas. Animals were then divided into tertiles based on their body fat rank: high, intermediate, and low (H, I, and L). Each group was further divided into 2 subgroups and then PVN injected with BDNF or control (artificial cerebrospinal fluid, aCSF) every other day for 3 wk. Energy intake (EI), body weight, and body composition were measured. At study's end, rats were killed to allow measurement of other metabolic indices. In parallel, another 12 rats were fed control diet (CD), PVN-cannulated and injected with aCSF. HFD exposure induced obesity, particularly in the H body fat group, with a significant increase in EI, body weight, fat mass, liver size, and serum glucose, triglycerides, insulin, and leptin. BDNF significantly reduced EI, body weight, body fat, lean mass, and serum metabolic indices. These BDNF effects were greatest in the H body fat group. These data indicate that BDNF reduced HFD-induced obesity and metabolic syndrome-like measures, and the animals with the most body fat had the most significant response to BDNF.

Brain-derived neurotrophic factor in the hypothalamic paraventricular nucleus increases energy expenditure by elevating metabolic rate

2007 ◽  
Vol 293 (3) ◽  
pp. R992-R1002 ◽  
Author(s):  
ChuanFeng Wang ◽  
Eric Bomberg ◽  
Charles Billington ◽  
Allen Levine ◽  
Catherine M. Kotz
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Food Intake ◽  
Energy Expenditure ◽  
Metabolic Rate ◽  
Paraventricular Nucleus ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Hypothalamic Paraventricular Nucleus ◽  
Sites Of Action

Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified. The hypothalamic paraventricular nucleus (PVN) is important in energy metabolism regulation, and expresses both BDNF and its receptor. We tested three hypotheses: 1) PVN BDNF reduces feeding and increases energy expenditure (EE), 2) PVN BDNF-enhanced thermogenesis results from increased spontaneous physical activity (SPA) and resting metabolic rate (RMR), and 3) PVN BDNF thermogenic effects are mediated, in part, by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5 μg) was injected into the PVN of Sprague-Dawley rats; and oxygen consumption, carbon dioxide production, food intake, and SPA were measured for 24 h in an indirect calorimeter. SPA was also measured in open-field activity chambers for 48 h after BDNF injection. Animals were killed 6 or 24 h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real-time PCR. BDNF significantly decreased food intake and body weight gain 24 h after injection. Heat production and RMR were significantly elevated for 7 h immediately after BDNF injection. BDNF had no effect on SPA, but increased UCP1 gene expression in BAT at 6 h, but not 24 h after injection. In conclusion, PVN BDNF reduces body weight by decreasing food intake and increasing EE consequent to increased RMR, which may be due, in part, to BAT UCP1 activity. These data suggest that the PVN is an important site of BDNF action to influence energy balance.

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