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首页> 外文期刊>The European Journal of Neuroscience >Mechanism of the medium-duration afterhyperpolarization in rat serotonergic neurons
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Mechanism of the medium-duration afterhyperpolarization in rat serotonergic neurons

机译：大鼠血清奈良菌神经元中持续后持续的机制

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摘要

Most serotonergic neurons display a prominent medium-duration afterhyperpolarization (mAHP), which is mediated by small-conductance Ca2+-activated K+ (SK) channels. Recent ex vivo and in vivo experiments have suggested that SK channel blockade increases the firing rate and/or bursting in these neurons. The purpose of this study was therefore to characterize the source of Ca2+ which activates the mAHP channels in serotonergic neurons. In voltage-clamp experiments, an outward current was recorded at -60 mV after a depolarizing pulse to +100 mV. A supramaximal concentration of the SK channel blockers apamin or (-)-bicuculline methiodide blocked this outward current. This current was also sensitive to the broad Ca2+ channel blocker Co2+ and was partially blocked by both ω-conotoxin and mibefradil, which are blockers of N-type and T-type Ca2+ channels, respectively. Neither blockers of other voltage-gated Ca2+ channels nor DBHQ, an inhibitor of Ca2+-induced Ca2+ release, had any effect on the SK current. In current-clamp experiments, mAHPs following action potentials were only blocked by ω-conotoxin and were unaffected by mibefradil. This was observed in slices from both juvenile and adult rats. Finally, when these neurons were induced to fire in an in vivo-like pacemaker rate, only ω-conotoxin was able to increase their firing rate (by ~30%), an effect identical to the one previously reported for apamin. Our results demonstrate that N-type Ca2+ channels are the only source of Ca2+ which activates the SK channels underlying the mAHP. T-type Ca2+ channels may also activate SK channels under different circumstances.
机译：大多数血清onOnergic神经元显示出突出的介质持续时间后渗透（MAHP），其由小导电CA2 +活化的K +（SK）通道介导。最近的前体内和体内实验表明SK通道阻断增加了这些神经元的烧制率和/或爆裂。因此，该研究的目的是表征Ca2 +的来源，其在血清oneronergic神经元中激活MaHP频道。在电压 - 钳位实验中，在将去极化脉冲到+100mV的+ 100mV之后将外电流记录在-60mV。 SK通道阻滞剂Apamin或（ - ） - Biculline Methiodide的SupraMaximal浓度阻挡了这种向外电流。该电流对宽CA2 +通道阻断剂CO2 +也敏感，并且部分地被ω-圆锥毒素和mibefradil封闭，它们分别是n型和T型CA2 +通道的阻挡剂。其他电压门控Ca2 +通道的阻滞剂也不是Ca2 +-诱导的Ca2 +释放的抑制剂，对SK电流有任何影响。在当前钳位实验中，MAHPS跟随动作电位仅被ω-conotoxin阻断，并且不受mimefradil的影响。这是从少年和成年大鼠的切片中观察到的。最后，当这些神经元诱导以体内的起搏器速率进行火，只有ω-芋头毒素能够增加烧制率（〜30％），其效果与先前报道的Apamin的效果相同。我们的结果表明，N型CA2 +通道是CA2 +的唯一来源，其激活MAHP下面的SK频道。 T型CA2 +通道还可以在不同情况下激活SK频道。

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