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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >The Downregulation of Somatic A-Type K+ Channels Requires the Activation of Synaptic NMDA Receptors in Young Hippocampal Neurons of Rats
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The Downregulation of Somatic A-Type K+ Channels Requires the Activation of Synaptic NMDA Receptors in Young Hippocampal Neurons of Rats

机译：体细胞A型K +通道的下调需要激活大鼠幼海马神经元中突触NMDA受体。

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The downregulation of A-type K+ channels (IA channels) accompanying enhanced somatic excitability can mediate epileptogenic conditions in mammalian central nervous system. As IA channels are dominantly targeted by dendritic and postsynaptic processings during synaptic plasticity, it is presumable that they may act as cellular linkers between synaptic responses and somatic processings under various excitable conditions. In the present study, we electrophysiologically tested if the downregulation of somatic IA channels was sensitive to synaptic activities in young hippocampal neurons. In primarily cultured hippocampal neurons (DIV 6~9), the peak of IA recorded by a whole-cell patch was significantly reduced by high KCl or exogenous glutamate treatment to enhance synaptic activities. However, the pretreatment of MK801 to block synaptic NMDA receptors abolished the glutamate-induced reduction of the IA peak, indicating the necessity of synaptic activation for the reduction of somatic IA. This was again confirmed by glycine treatment, showing a significant reduction of the somatic IA peak. Additionally, the gating property of IA channels was also sensitive to the activation of synaptic NMDA receptors, showing the hyperpolarizing shift in inactivation kinetics. These results suggest that synaptic LTP possibly potentiates somatic excitability via downregulating IA channels in expression and gating kinetics. The consequential changes of somatic excitability following the activity-dependent modulation of synaptic responses may be a series of processings for neuronal functions to determine outputs in memory mechanisms or pathogenic conditions.
机译：伴随体细胞兴奋性增强的A型K + 通道（I A 通道）的下调可以介导哺乳动物中枢神经系统的致痫性疾病。由于I A 通道在突触可塑性过程中主要受到树突和突触后加工的靶向，因此推测它们可能在各种兴奋条件下充当突触反应和体细胞加工之间的细胞连接体。在本研究中，我们进行了电生理学测试，证明体细胞I A 通道的下调是否对年轻海马神经元的突触活动敏感。在原代培养的海马神经元（DIV 6〜9）中，高KCl或外源谷氨酸处理可显着降低全细胞膜片记录的I A 峰，从而增强突触活性。然而，MK801阻断突触NMDA受体的预处理取消了谷氨酸诱导的I A 峰的降低，表明突触激活对于降低体细胞I A 的必要性。 。甘氨酸处理再次证实了这一点，表明体细胞I A 峰显着降低。此外，I A 通道的门控特性也对突触NMDA受体的激活敏感，显示了失活动力学的超极化转变。这些结果表明，突触LTP可能通过下调表达和门控动力学中的I A 通道来增强体细胞兴奋性。突触反应的活动依赖性调节后，躯体兴奋性的相应变化可能是一系列神经元功能处理，以确定记忆机制或致病条件下的输出。

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