...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Evidence for protein tyrosine phosphatase, tyrosine kinase, and G-protein regulation of the parallel fiber metabotropic slow EPSC of rat cerebellar Purkinje neurons.
【24h】

Evidence for protein tyrosine phosphatase, tyrosine kinase, and G-protein regulation of the parallel fiber metabotropic slow EPSC of rat cerebellar Purkinje neurons.

机译：大鼠小脑浦肯野神经元的平行纤维代谢慢EPSC的蛋白酪氨酸磷酸酶，酪氨酸激酶和G蛋白调节的证据。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The slow EPSP (sEPSP) or slow EPSC (sEPSC) at parallel fiber to Purkinje neuron synapses is attributable to a nonselective cation channel coupled to activation of metabotropic type 1 glutamate receptors (mGluR1s). Photorelease of L-glutamate in 1 msec from 4-methoxy-7-nitroindolinyl-or 7-nitroindolinyl-caged glutamate in cerebellar slices was used to isolate and study postsynaptic mechanisms coupling mGluR1 to the cation channel. L-Glutamate immediately activated a glutamate transporter current, followed by the slow mGluR1-activated conductance. Inhibitors of kinases, phosphatases, and G-proteins were tested on the peak glutamate-evoked currents. No effects of the inhibitors were seen on the initial glutamate transporter currents. In contrast, the later mGluR1 currents were either unaffected or enhanced by the protein tyrosine kinase (PTK) inhibitors PP1, K252a, and staurosporine were diminished or blocked by phosphatase inhibitors but were unaffected by inhibitors of serine-threonine kinases PKA, PKC,or PKG. The selective src-PTK inhibitor PP1 (10 microm intracellularly) potentiated submaximal mGluR1 currents evoked by low L-glutamate concentrations but had no effect on maximal responses (80 or 160 microm L-glutamate). L-Glutamate-evoked mGluR1 currents and parallel fiber sEPSCs were reversibly and completely inhibited by protein tyrosine phosphatase (PTP) inhibitor bpV(phen) (50-200 microm) and by nonselective phosphatase inhibitor orthovanadate (0.5 or 1 mm). mGluR1 currents were completely inhibited by GDPbetaS applied intracellularly (5 mm). The results confirm a role for a GTPase postsynaptically, show that tyrosine phosphorylation inhibits mGluR1 coupling to the channel, and show that PTPs increase activation by tyrosine dephosphorylation most likely upstream of the sEPSP cation channel.
机译：平行纤维与浦肯野神经元突触处的慢EPSP（sEPSP）或慢EPSC（sEPSC）归因于与选择性代谢型1型谷氨酸受体（mGluR1s）激活偶联的非选择性阳离子通道。小脑切片中的4-甲氧基-7-硝基吲哚基-或7-硝基吲哚基笼中的谷氨酸在1毫秒内释放L-谷氨酸的光释放，用于分离和研究将mGluR1偶联至阳离子通道的突触后机制。 L-谷氨酸立即激活谷氨酸转运蛋白电流，随后是缓慢的mGluR1激活的电导。在谷氨酸诱发的峰值电流上测试了激酶，磷酸酶和G蛋白的抑制剂。没有观察到抑制剂对初始谷氨酸转运蛋白电流的影响。相反，后来的mGluR1电流不受蛋白酪氨酸激酶（PTK）抑制剂PP1，K252a的影响或增强，而星形孢菌素则被磷酸酶抑制剂抑制或阻断，但不受丝氨酸-苏氨酸激酶PKA，PKC或PKG抑制剂的影响。选择性src-PTK抑制剂PP1（细胞内10微米）可通过低L-谷氨酸浓度引起亚最大mGluR1电流，但对最大响应（80或160微米L-谷氨酸）没有影响。 L-谷氨酸诱发的mGluR1电流和平行纤维sEPSC受蛋白质酪氨酸磷酸酶（PTP）抑制剂bpV（phen）（50-200 microm）和非选择性磷酸酶抑制剂原钒酸盐（0.5或1 mm）可逆和完全抑制。 mGluR1电流被细胞内施用的GDPbetaS完全抑制（5毫米）。结果证实了突触后GTP酶的作用，表明酪氨酸磷酸化抑制mGluR1偶联至通道，并表明PTP通过酪氨酸脱磷酸作用最有可能在sEPSP阳离子通道上游增加活化。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号