Teo James T H, Bentley Graham, Lawrence Philip, Soltesz Fruzsina, Miller Sam, Willé David, McHugh Simon, Dodds Chris, Lu Bai, Croft Rodney J, Bullmore Edward T, Nathan Pradeep J
Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, University College London, UK.
Medicines Discovery and Development, GlaxoSmithKline Clinical Unit Cambridge, UK.
Int J Neuropsychopharmacol. 2014 May;17(5):705-13. doi: 10.1017/S1461145713001636. Epub 2014 Jan 9.
The brain-derived neurotropic factor (BDNF) Val66Met polymorphism has been associated with abnormalities of synaptic plasticity in animal models, and abnormalities in motor cortical plasticity have also been described in humans using transcranial direct current stimulation. No study has yet been done on plasticity in non-motor regions, and the effect of two Met alleles (i.e. 'Met dose') is not well understood. We studied the effect of the BDNF Val66Met polymorphism on the after-effects of transcranial direct current stimulation and tetanic auditory stimulation in 65 subjects (23; Val66Val, 22; Val66Met and 20; Met66Met genotypes). In the first session, motor evoked potentials (MEP) were recorded under stereotaxic guidance for 90 min after 9 min of anodal transcranial direct current stimulation (TDCS). In the second session, auditory-evoked potentials (AEP) were recorded before and after 2 min of auditory 13 Hz tetanic stimulation. There was a difference in MEP facilitation post-TDCS comparing Met carriers with non-Met carriers, with Met carriers having a modest late facilitation at 30-90 min. There was no difference in responses between Val66Met genotype and Met66Met genotype subjects. Tetanic auditory stimulation also produced late facilitation of N1-P2 AEP at 25 min, but there was no apparent effect of genetic status. This study indicates that Met66Met carriers behave like Val66Met carriers for TDCS-induced plasticity, and produce a late facilitation of MEPs. Auditory cortical plasticity was not affected by the BDNF Val66Met polymorphism. This study sheds light on the differences between auditory and motor cortical plasticity and the role of the BDNF Val66Met polymorphism.
脑源性神经营养因子（BDNF）Val66Met多态性在动物模型中与突触可塑性异常有关，并且在人类中使用经颅直流电刺激也描述了运动皮质可塑性异常。尚未有关于非运动区域可塑性的研究，并且两个Met等位基因的作用（即“Met剂量”）尚未得到很好的理解。我们研究了BDNF Val66Met多态性对65名受试者（23名；Val66Val基因型，22名；Val66Met基因型和20名；Met66Met基因型）经颅直流电刺激和强直听觉刺激后效应的影响。在第一阶段，在阳极经颅直流电刺激（TDCS）9分钟后，在立体定向引导下记录90分钟的运动诱发电位（MEP）。在第二阶段，在13Hz听觉强直刺激2分钟前后记录听觉诱发电位（AEP）。比较Met携带者与非Met携带者，TDCS后MEP易化存在差异，Met携带者在30 - 90分钟有适度的晚期易化。Val66Met基因型和Met66Met基因型受试者之间的反应没有差异。强直听觉刺激在25分钟时也产生了N1 - P2 AEP的晚期易化，但遗传状态没有明显影响。这项研究表明，对于TDCS诱导的可塑性，Met66Met携带者的表现与Val66Met携带者相似，并产生MEP的晚期易化。听觉皮质可塑性不受BDNF Val66Met多态性的影响。这项研究揭示了听觉和运动皮质可塑性之间的差异以及BDNF Val66Met多态性的作用。
