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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Experiments to test the role of phosphatidylinositol 4,5-bisphosphate in neurotransmitter-induced M-channel closure in bullfrog sympathetic neurons.
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Experiments to test the role of phosphatidylinositol 4,5-bisphosphate in neurotransmitter-induced M-channel closure in bullfrog sympathetic neurons.

机译：实验测试磷脂酰肌醇4,5-二磷酸在牛蛙交感神经元的神经递质诱导的M通道闭合中的作用。

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摘要

Various neurotransmitters excite neurons by suppressing a ubiquitous, voltage-dependent, noninactivating K+ conductance called the M-conductance (gM). In bullfrog sympathetic ganglion neurons the suppression of gM by the P2Y agonist ATP involves phospholipase C (PLC). The present results are consistent with the involvement of the lipid and inositol phosphate cycles in the effects of both P2Y and muscarinic cholinergic agonists on gM. Impairment of resynthesis of phosphatidylinositol 4,5-bisphosphate (PIP2) with the phosphatidylinositol 4-kinase inhibitor wortmannin (10 microm) slowed or blocked the recovery of agonist-induced gM suppression. This effect could not be attributed to an action of wortmannin on myosin light chain kinase or on phosphatidylinositol 3-kinase. Inhibition of PIP2 synthesis at an earlier point in the lipid cycle by the use of R59022 (40 microm) to inhibit diacylglycerol kinase also slowed the rate of recovery of successive ATP responses. This effect required several applications of agonist to deplete levels of various phospholipid intermediates in the lipid cycle. PIP2 antibodies attenuated the suppression of gM by agonists. Intracellular application of 20 microm PIP2 slowed the rundown of KCNQ2/3 currents expressed in COS-1 or tsA-201 cells, and 100 microm PIP2 produced a small potentiation of native M-current bullfrog sympathetic neurons. These are the results that might be expected if agonist-induced activation of PLC and the concomitant depletion of PIP2 contribute to the excitatory action of neurotransmitters that suppress gM.
机译：各种神经递质通过抑制普遍存在的电压依赖性非灭活K +电导（称为M电导（gM））来激发神经元。在牛蛙交感神经节神经元中，P2Y激动剂ATP对gM的抑制作用涉及磷脂酶C（PLC）。本结果与脂质和肌醇磷酸循环参与P2Y和毒蕈碱胆碱能激动剂对gM的作用一致。磷脂酰肌醇4-激酶抑制剂渥曼青霉素（10 microm）对磷脂酰肌醇4,5-双磷酸酯（PIP2）的再合成损害减慢或阻止了激动剂诱导的gM抑制的恢复。该作用不能归因于渥曼青霉素对肌球蛋白轻链激酶或磷脂酰肌醇3-激酶的作用。通过使用R59022（40微米）抑制二酰基甘油激酶在脂质循环的较早阶段抑制PIP2的合成，也减缓了连续ATP反应的恢复速度。这种作用需要激动剂的几次应用以减少脂质循环中各种磷脂中间体的水平。 PIP2抗体减弱了激动剂对gM的抑制作用。胞内应用20微米PIP2可以减慢在COS-1或tsA-201细胞中表达的KCNQ2 / 3电流的衰减，而100微米PIP2可以产生少量的天然M电流牛蛙交感神经元。如果激动剂诱导的PLC活化和PIP2的同时耗竭有助于抑制gM的神经递质的兴奋作用，那么这些结果是可以预期的。

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