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BDNF Interacts with Endocannabinoids to Regulate Cocaine-Induced Synaptic Plasticity in Mouse Midbrain Dopamine Neurons
Zhong, Peng1; Liu, Yong1,2; Hu, Ying1; Wang, Tong1; Zhao, Yong-ping1,3; Liu, Qing-song1
关键词Bdnf Cocaine Conditioned Place Preference Dsi Endocannabinoid I-ltd
刊名JOURNAL OF NEUROSCIENCE
2015-03-11
DOI10.1523/JNEUROSCI.2924-14.2015
35期:10页:4469-4481
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences
资助者National Institutes of Health ; Research and Education Initiative Fund, a component of the Advancing a Healthier Wisconsin endowment at the Medical College of Wisconsin ; National Institutes of Health ; Research and Education Initiative Fund, a component of the Advancing a Healthier Wisconsin endowment at the Medical College of Wisconsin
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]VENTRAL TEGMENTAL AREA ; CONDITIONED-PLACE PREFERENCE ; METABOTROPIC GLUTAMATE RECEPTORS ; MEDIAL PREFRONTAL CORTEX ; LONG-TERM POTENTIATION ; ENDOGENOUS CANNABINOIDS ; NEUROTROPHIC FACTOR ; NUCLEUS-ACCUMBENS ; PHOSPHOLIPASE-C ; INHIBITORY SYNAPSES
英文摘要

Brain-derived neurotrophic factor (BDNF) and endocannabinoids (eCBs) have been individually implicated in behavioral effects of cocaine. The present study examined how BDNF-eCB interaction regulates cocaine-induced synaptic plasticity in the ventral tegmental area and behavioral effects. We report that BDNF and selective tyrosine kinase receptor B (TrkB) agonist 7,8-dihydroxyflavone (DHF) activated the TrkB receptor to facilitate two forms of eCB-mediated synaptic depression, depolarization-induced suppression of inhibition (DSI), and long-term depression (I-LTD) of IPSCs in ventral tegmental area dopamine neurons in mouse midbrain slices. The facilitation appears to be mediated by an increase in eCB production via phospholipase C gamma pathway, but not by an increase in CB1 receptor responsiveness or a decrease in eCB hydrolysis. Using Cre-loxP technology to specifically delete BDNF in dopamine neurons, we showed that eCB-mediated I-LTD, cocaine-induced reduction of GABAergic inhibition, and potentiation of glutamatergic excitation remained intact in wild-type control mice, but were impaired in BDNF conditional knock-out mice. We also showed that cocaine-induced conditioned place preference was attenuated in BDNF conditional knock-out mice, in vivo pretreatments with DHF before place conditioning restored cocaine conditioned place preference in these mice, and the behavioral effect of DHF was blocked by a CB1 receptor antagonist. Together, these results suggest that BDNF in dopamine neurons regulates eCB responses, cocaine-induced synaptic plasticity, and associative learning.

语种英语
所属项目编号DA035217 ; MH101146
资助者National Institutes of Health ; Research and Education Initiative Fund, a component of the Advancing a Healthier Wisconsin endowment at the Medical College of Wisconsin ; National Institutes of Health ; Research and Education Initiative Fund, a component of the Advancing a Healthier Wisconsin endowment at the Medical College of Wisconsin
WOS记录号WOS:000352199900030
引用统计
被引频次:16[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/53853
专题北京大学第二临床医学院
作者单位1.Med Coll Wisconsin, Dept Pharmacol & Toxicol, Milwaukee, WI 53226 USA
2.Xuzhou Med Coll, Jiangsu Key Lab Brain Dis Bioinformat, Res Ctr Biochem & Mol Biol, Xuzhou 221002, Jiangsu, Peoples R China
3.Peking Univ, Peoples Hosp, Reprod Ctr, Beijing 100871, Peoples R China
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GB/T 7714
Zhong, Peng,Liu, Yong,Hu, Ying,et al. BDNF Interacts with Endocannabinoids to Regulate Cocaine-Induced Synaptic Plasticity in Mouse Midbrain Dopamine Neurons[J]. JOURNAL OF NEUROSCIENCE,2015,35(10):4469-4481.
APA Zhong, Peng,Liu, Yong,Hu, Ying,Wang, Tong,Zhao, Yong-ping,&Liu, Qing-song.(2015).BDNF Interacts with Endocannabinoids to Regulate Cocaine-Induced Synaptic Plasticity in Mouse Midbrain Dopamine Neurons.JOURNAL OF NEUROSCIENCE,35(10),4469-4481.
MLA Zhong, Peng,et al."BDNF Interacts with Endocannabinoids to Regulate Cocaine-Induced Synaptic Plasticity in Mouse Midbrain Dopamine Neurons".JOURNAL OF NEUROSCIENCE 35.10(2015):4469-4481.
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