Ikeda Takamitsu, Tamura Naohiro, Matsuki Norio, Yamada Maki K
Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Bunkyo-ku, Tokyo, Japan.
Neuroreport. 2006 Dec 18;17(18):1847-51. doi: 10.1097/WNR.0b013e328011592c.
Brain-derived neurotrophic factor has been implicated in higher cognitive functions, and several neurological and psychiatric disorders. Recently, a variant brain-derived neurotrophic factor (BDNFMet), having a substitution referred to as Val66Met, was reported as a product of a bdnf allele with a common single nucleotide polymorphism. It has been reported that BDNFMet is impaired in its potential for activity-dependent release. We sparsely transfected cultured hippocampal neurons with BDNFMet or wild-type BDNFVal cDNAs and examined the amount of GABA-synthetic enzyme glutamic acid decarboxylase 65 (GAD65) in the adjacent region, probably in the GABAergic synapses. BDNFMet transfection increased the GAD65 level to the same extent as transfection with BDNFVal. Our findings suggest that the activity-independent secretion of brain-derived neurotrophic factor may be sufficient to induce inhibitory regulation.
脑源性神经营养因子与高级认知功能以及多种神经和精神疾病有关。最近，一种变异的脑源性神经营养因子（BDNFMet），具有一个称为Val66Met的替换，被报道为一个具有常见单核苷酸多态性的脑源性神经营养因子等位基因的产物。据报道，BDNFMet在其活性依赖性释放潜力方面存在缺陷。我们用BDNFMet或野生型BDNFVal cDNA对培养的海马神经元进行稀疏转染，并检测相邻区域（可能是GABA能突触）中GABA合成酶谷氨酸脱羧酶65（GAD65）的量。BDNFMet转染使GAD65水平升高到与BDNFVal转染相同的程度。我们的研究结果表明，脑源性神经营养因子的非活性依赖性分泌可能足以诱导抑制性调节。
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