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Am J Physiol Regul Integr Comp Physiol (June 20, 2007). doi:10.1152/ajpregu.00011.2007
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Submitted on January 9, 2007
Accepted on June 14, 2007

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

ChuanFeng Wang1*, Eric Bomberg2, Charles Billington3, Allen Levine4, and Catherine M. Kotz5

1 Research Services, Veterans Affairs Medical Center, Minneapolis, Minnesota, United States; Food Science and Nutrition, University of Minnesota, St. Paul, Minnesota, United States
2 Research Services, Veterans Affairs Medical Center, Minneapolis, Minnesota, United States
3 Research Services, Veterans Affairs Medical Center, Minneapolis, Minnesota, United States; Minnesota Obesity Center, Minneapolis, Minnesota, United States
4 Research Services, Veterans Affairs Medical Center, Minneapolis, Minnesota, United States; Minnesota Obesity Center, Minneapolis, Minnesota, United States; Food Science and Nutrition, University of Minnesota, St. Paul, Minnesota, United States
5 Geriatric Research, Education and Clinical Center (11G), Veterans Affairs Medical Center, Minneapolis, Minnesota, United States; Minnesota Obesity Center, Minneapolis, Minnesota, United States; Food Science and Nutrition, University of Minnesota, St. Paul, Minnesota, United States; Graduate Program in Neuroscience, University of Minnesota, Minneapolis, Minnesota, United States

* To whom correspondence should be addressed. E-mail: cwang{at}umn.edu.

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, 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 non-deprived rats significantly decreased feeding and body weight gain within the 0-24 h and 24-48 h post-injection 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 important site of action for BDNF in its effects on energy metabolism. Further, BDNF appears to interact with NPY in its anorectic actions, although a direct effect on NPY remains to be established.




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