Activation of the Tonic GABAC Receptor Current in Retinal Bipolar Cell Terminals by Nonvesicular GABA Release
Activation of the Tonic GABAC Receptor Current in Retinal Bipolar Cell Terminals by Nonvesicular GABA Release
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DOI：
10.1152/jn.00285.2009
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发表时间：
2009-08-01
影响因子：
2.5
通讯作者：
Palmer, M. J.
中科院分区：
文献类型：
--
作者：
Jones, S. M.;Palmer, M. J.
Jones SM，Palmer MJ.通过非囊泡GABA释放激活视网膜双极细胞终末的强直性GABA（C）受体电流。J Neurophysiol 102：691-699，2009.首次发表于2009年6月3日; doi：10.1152/jn.00285.2009。在视网膜的第二突触层内，双极细胞（BC）输出到神经节细胞由到BC轴突终末的抑制性输入调节。GABA（A）受体（GABA（A）Rs）介导BC终末中的快速突触电流，而GABA（C）受体（GABA（C）Rs）介导缓慢诱发电流和紧张电流，其受GAT-1 GABA转运蛋白的强烈调节。我们已经使用电压钳记录从BC终端在金鱼视网膜切片，以确定源的GABA激活这些电流。用Concanamycin A或破伤风毒素抑制囊泡释放可显著抑制GABA（A）R抑制性突触后电流和谷氨酸诱发的GABA（A）R和GABA（C）R电流，但不降低紧张性GABA（C）R电流，该电流也不依赖于细胞外Ca 2+。紧张性电流强烈增强抑制GABA转氨酶，在正常和Ca 2 +-无条件下，并激活外源性牛磺酸，但抑制牛磺酸运输的影响不大。紧张电流不受GAT-2/3抑制，并增强GAT-1抑制，即使在没有囊泡释放，表明它是不可能诱发的GABA转运逆转或环境GABA。此外，GABA的释放似乎不通过半通道或P2 X（7）受体发生。因此，BC终末表现出两种形式的GABA（C）R介导的抑制，由囊泡和非囊泡GABA释放激活，这可能在视觉信号处理中具有不同的功能。BC终末的紧张性GABA（C）R电流表现出与脑中的紧张性GABA（A）R和谷氨酸受体电流相似的性质。
Jones SM, Palmer MJ. Activation of the tonic GABA(C) Receptor current in retinal bipolar cell terminals by nonvesicular GABA release. J Neurophysiol 102: 691-699, 2009. First published June 3, 2009; doi:10.1152/jn.00285.2009. Within the second synaptic layer of the retina, bipolar cell (BC) output to ganglion cells is regulated by inhibitory input to BC axon terminals. GABA(A) Receptors (GABA(A)Rs) mediate rapid synaptic currents in BC terminals, whereas GABA(C) receptors (GABA(C)Rs) mediate slow evoked currents and a tonic current, which is strongly regulated by GAT-1 GABA transporters. We have used voltage-clamp recordings from BC terminals in goldfish retinal slices to determine the source of GABA for activation of these currents. Inhibition of vesicular release with concanamycin A or tetanus toxin significantly inhibited GABA(A)R inhibitory postsynaptic currents and glutamate-evoked GABA(A)R and GABA(C)R currents but did not reduce the tonic GABA(C)R current, which was also not dependent on extracellular Ca2+. The tonic current was strongly potentiated by inhibition of GABA transaminase, under both normal and Ca2+-free conditions, and was activated by exogenous taurine; however inhibition of taurine transport had little effect. The tonic current was unaffected by GAT-2/3 inhibition and was potentiated by GAT-1 inhibition even in the absence of vesicular release, indicating that it is unlikely to be evoked by reversal of GABA transporters or by ambient GABA. In addition, GABA release does not appear to occur via hemichannels or P2X(7) receptors. BC terminals therefore exhibit two forms of GABA(C)R-mediated inhibition, activated by vesicular and by nonvesicular GABA release, which are likely to have distinct functions in visual signal processing. The tonic GABA(C)R current in BC terminals exhibits similar properties to tonic GABA(A)R and glutamate receptor currents in the brain.