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首页> 外文期刊>Journal of Neurophysiology >Ca~(2+)-activated ion currents triggered by ryanodine receptor-mediated Ca~(2+) release control firing of inhibitory neurons in the prepositus hypoglossi nucleus
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Ca~(2+)-activated ion currents triggered by ryanodine receptor-mediated Ca~(2+) release control firing of inhibitory neurons in the prepositus hypoglossi nucleus

机译：ryanodine受体介导的Ca〜（2+）触发的Ca〜（2+）激活的离子电流释放抑制垂体前突肌核中抑制性神经元的放电。

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摘要

Spontaneous miniature outward currents (SMOCs) are known to exist in smooth muscles and peripheral neurons, and evidence for the presence of SMOCs in central neurons has been accumulating. SMOCs in central neurons are induced through Ca~(2+)-activated K~+ (K_(Ca)) channels, which are activated through Ca~(2+)-induced Ca~(2+) release from the endoplasmic reticulum via ryanodine receptors (RyRs). Previously, we found that some neurons in the prepositus hypoglossi nucleus (PHN) showed spontaneous outward currents (SOCs). In the present study, we used whole cell recordings in slice preparations of the rat brain stem to investigate the following: 1) the ionic mechanisms of SOCs, 2) the types of neurons exhibiting frequent SOCs, and 3) (he effect of Ca~(2+)-activated conductance on neuronal firing. Pharmacological analyses revealed that SOCs were induced via the activation of small-conductance-type K_(Ca) (SK) channels and RyRs, indicating that SOCs correspond to SMOCs. An analysis of the voltage responses to current pulses of the fluorescence-expressing inhibitory neurons of transgenic rats revealed that inhibitory neurons frequently exhibited SOCs. Abolition of SOCs via blockade of SK channels enhanced the frequency of spontaneous firing of inhibitory PHN neurons. However, abolition of SOCs via blockade of RyRs reduced the firing frequency and hyperpolarized the membrane potential. Similar reductions in firing frequency and hyperpolarization were also observed when Ca~(2+)-activated nonselective cation (CAN) channels were blocked. These results suggest that, in inhibitory neurons in the PHN, Ca~(2+) release via RyRs activates SK and CAN channels, and these channels regulate spontaneous firing in a complementary manner.
机译：已知自发的微型外向电流（SMOC）存在于平滑肌和周围神经元中，并且在中枢神经元中存在SMOC的证据正在积累。中枢神经元中的SMOCs通过Ca〜（2+）激活的K〜+（K_（Ca））通道诱导，该通道通过Ca〜（2+）诱导的Ca〜（2+）从内质网释放而被激活。 ryanodine受体（RyRs）。以前，我们发现在垂体前丘脑核（PHN）中某些神经元显示出自发的外向电流（SOC）。在本研究中，我们使用大鼠脑干切片制剂中的全细胞记录来研究以下内容：1）SOC的离子机制，2）表现出频繁SOC的神经元类型，以及3）（Ca〜 （2+）激活神经元放电的电导。药理分析表明，SOC是通过激活小电导型K_（Ca）（SK）通道和RyRs诱导的，表明SOC与SMOC对应。转基因大鼠对表达荧光的抑制性神经元电流脉冲的反应表明抑制性神经元经常表现出SOC，通过阻断SK通道取消SOC可以增加抑制性PHN神经元自发放电的频率，但是通过阻断RyRs可以消除SOC。降低了激发频率，并使膜电位超极化;当Ca〜（2+）活化的非选择性阳离子时，激发频率和超极化也有类似的降低（CAN）频道被阻止。这些结果表明，在PHN中的抑制神经元中，经由RyRs释放的Ca〜（2+）激活SK和CAN通道，并且这些通道以互补的方式调节自发放电。

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