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首页> 外文期刊>The European Journal of Neuroscience >Calcium-regulated potassium currents secure respiratory rhythm generation after loss of glycinergic inhibition.
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Calcium-regulated potassium currents secure respiratory rhythm generation after loss of glycinergic inhibition.

机译：失钙抑制后，钙调节的钾电流可确保呼吸节律的产生。

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摘要

Mutant oscillator mice (Glra1(spd -/-)) are characterized by a developmental loss of glycinergic inhibition. These mice die during the third postnatal week presumably due to gradually increasing disturbances of breathing and motor behaviour. Some irregular rhythmic respiratory activity, however, is persevered until they die. Here we analysed cellular mechanisms that compensate for the loss of glycinergic inhibition and contribute to the maintenance of the respiratory rhythm. In a medullary slice preparation including the pre-Botzinger complex we performed a comparative analysis of after-hyperpolarizations following action potentials (AP-AHP) and burst discharges (burst-AHP) in identified respiratory neurons from oscillator and control mice. Both AHP forms were increased in neurons from oscillator mice. These changes were combined with an augmented adaptation of firing frequency. Assuming that oscillator mice might upregulate calcium-activated K currents (BKCa) in compensation for the loss of glycinergic inhibition, we blocked the big KCa conductances with iberiotoxin and verified that the respiratory rhythm was indeed arrested by BK channel blockade.
机译：突变型振荡器小鼠（Glra1（spd-/-））的特征在于对甘氨酸抑制作用的发育丧失。这些小鼠死后第三周死亡，大概是由于呼吸和运动行为的逐渐增加所致。但是，一些不规则的节律性呼吸活动会持续到死亡。在这里，我们分析了补偿甘氨酸抑制作用丧失并有助于维持呼吸节律的细胞机制。在包括博茨灵前体复合物的髓样切片制剂中，我们对振荡器和对照小鼠中识别出的呼吸神经元的动作电位（AP-AHP）和爆发放电（burst-AHP）后的超极化后进行了比较分析。振荡器小鼠的神经元中两种AHP形式均增加。这些变化与点火频率的增强适应性相结合。假设振荡器小鼠可能通过上调钙激活的K电流（BKCa）来补偿失去的甘氨酸抑制作用，我们用纤毛毒素阻断了大的KCa电导，并验证了呼吸节律确实被BK通道阻滞所阻止。

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