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首页> 外文期刊>The Journal of Physiology >Voltage-dependent amplification of synaptic inputs in respiratory motoneurones
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Voltage-dependent amplification of synaptic inputs in respiratory motoneurones

机译:呼吸运动神经元中突触输入的电压依赖性扩增

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The role of persistent inward currents (PICs) in cat respiratory motoneurones (phrenic inspiratory and thoracic expiratory) was investigated by studying the voltage-dependent amplification of central respiratory drive potentials (CRDPs), recorded intracellularly, with action potentials blocked with the local anaesthetic derivative, QX-314. Decerebrate unanaesthetized or barbiturate-anaesthetized preparations were used. In expiratory motoneurones, plateau potentials were observed in the decerebrates, but not under anaesthesia. For phrenic motoneurones, no plateau potentials were observed in either state (except in one motoneurone after the abolition of the respiratory drive by means of a medullary lesion), but all motoneurones showed voltage-dependent amplification of the CRDPs, over a wide range of membrane potentials, too wide to result mainly from PIC activation. The measurements of the amplification were restricted to the phase of excitation, thus excluding the inhibitory phase. Amplification was found to be greatest for the smallest CRDPs in the lowest resistance motoneurones and was reduced or abolished following intracellular injection of the NMDA channel blocker, MK-801. Plateau potentials were readily evoked in non-phrenic cervical motoneurones in the same (decerebrate) preparations. We conclude that the voltage-dependent amplification of synaptic excitation in phrenic motoneurones is mainly the result of NMDA channel modulation rather than the activation of Ca 2+ channel mediated PICs, despite phrenic motoneurones being strongly immunohistochemically labelled for Ca V1.3 channels. The differential PIC activation in different motoneurones, all of which are Ca V1.3 positive, leads us to postulate that the descending modulation of PICs is more selective than has hitherto been believed.
机译:通过研究细胞内记录的中央呼吸驱动电位(CRDP)的电压依赖性扩增,研究了持续内向电流(PIC)在猫呼吸运动神经元((吸和胸呼气)中的作用,并用局麻药阻断了动作电位,QX-314。使用未麻醉的去脑小儿或巴比妥酸盐麻醉的制剂。在呼气运动神经元中,在大脑中观察到平台电位,但在麻醉下未观察到平台电位。对于运动神经元,在两种状态下均未观察到平台电位(除了通过髓性病变取消呼吸驱动后的一个运动神经元),但是所有运动神经元在宽范围的膜上均显示出电压依赖性的CRDP扩增。电位太宽,无法主要由PIC激活引起。扩增的测量仅限于激发阶段,因此不包括抑制阶段。发现在抵抗力最低的运动神经元中,最小的CRDP的扩增最大,并且在细胞内注射NMDA通道阻滞剂MK-801后被减少或取消。在相同(去脑子)制剂中,非non宫颈运动神经元容易诱发高原电位。我们得出结论,despite神经元中突触兴奋的电压依赖性扩增主要是NMDA通道调节的结果,而不是Ca 2+通道介导的PIC的激活,尽管神经元被Ca V1.3通道强烈免疫组化标记。在所有不同的运动神经元中,PIC的差异激活都是Ca V1.3阳性,这使我们推测PIC的降序调节比迄今所认为的更具选择性。

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