Rapid modulation of inhibitory synaptic currents in cerebellar Purkinje cells by BDNF
Rapid modulation of inhibitory synaptic currents in cerebellar Purkinje cells by BDNF
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DOI：
10.1002/syn.20170
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发表时间：
2005-09-15
期刊：
影响因子：
2.3
通讯作者：
Drake-Baumann, R
中科院分区：
文献类型：
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作者：
Drake-Baumann, R
本研究探讨了外源性BDNF对小脑浦肯野细胞抑制性突触电流的急性效应。采用不连续单电极电压钳（dSEVC）技术，在体外培养20-30天的细胞中记录微小抑制性突触后电流（mIPSC）。BDNF的影响进行了研究，在未经处理的控制文化和文化，其中内源性水平的BDNF减少慢性阻滞神经活动与河豚毒素（TTX）。慢性活动剥夺并没有改变浦肯野细胞中mIPSC的振幅，急性应用BDNF（50 ng/ml）的浦肯野细胞在TTX处理的培养物显着增强mIPSC的振幅和频率。相比之下，急性应用BDNF（50 ng/ml）在对照神经元中对mIPSC活性没有产生显著变化。在较高浓度的BDNF（100 ng/ml）下，在对照神经元中也观察到对mIPSC活性的类似作用。用酪氨酸激酶抑制剂K252 a预孵育小脑培养物，有效地阻断了BDNF对mIPSCs的作用。这些结果表明，功能性抑制性突触的神经活动的情况下，和TrkB受体的激活BDNF调节抑制性神经传递浦肯野细胞在突触前和突触后的网站。
The present study examined the acute effects of exogenous BDNF on inhibitory synaptic currents in Purkinje cells in cerebellar cultures. Miniature inhibitory postsynaptic currents (mIPSCs) were recorded in cultures (20-30 days in vitro), using discontinuous single electrode voltage clamp (dSEVC) technique. The effects of BDNF were studied in untreated control cultures and in cultures in which the endogenous levels of BDNF were decreased by chronic block of neural activity with tetrodotoxin (TTX). Chronic activity deprivation did not alter the amplitude of mIPSCs in Purkinje cells, and acute application of BDNF (50 ng/ml) to Purkinje cells in TTX-treated cultures significantly potentiated the amplitude and frequency of mIPSCs. By contrast, acute application of BDNF (50 ng/ml) produced no significant changes on mIPSC activity in control neurons. At higher concentrations of BDNF (100 ng/ml), comparable effects on mIPSC activity were also observed in control neurons. Preincubation of cerebellar cultures with K252a, an inhibitor of tyrosine kinases, effectively blocked the effects of BDNF on mIPSCs. These results indicate that functional inhibitory synapses develop in the absence of neural activity, and that activation of TrkB receptors by BDNF modulates inhibitory neurotransmission in Purkinje cells at both pre- and postsynaptic sites.