KCNQ Current Contributes to Inspiratory Burst Termination in the Pre-Bötzinger Complex of Neonatal Rats in vitro.

KCNQ Current Contributes to Inspiratory Burst Termination in the Pre-Bötzinger Complex of Neonatal Rats in vitro.
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DOI:
10.3389/fphys.2021.626470
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发表时间:
2021
影响因子:
4
通讯作者:
Funk GD
Funk GD
中科院分区:
医学2区
文献类型:
--
作者:
Revill AL;Katzell A;Del Negro CA;Milsom WK;Funk GD

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腹侧延髓的前 Bötzinger 复合体 (preBötC) 产生哺乳动物吸气呼吸节律。当在外植体中分离并剥夺突触抑制时,preBötC 继续产生与吸气相关的节律。爆发产生的机制已经被研究了几十年,但负责爆发终止的细胞和突触机制却受到较少的关注。 KCNQ 介导的 K+ 电流有助于其他系统中的爆发终止,其转录本在 preBötC 神经元中表达。因此,我们测试了 KCNQ 通道也有助于 preBötC 中突发终止的假设。我们在保留呼吸节律的新生大鼠切片的 preBötC 吸气神经元中记录了类似 KCNQ 的电流。用 XE991 或利诺吡啶(通过灌注或局部应用)阻断 KCNQ 通道可使吸气爆发持续时间增加 2 至 3 倍。相比之下,用瑞替加滨激活 KCNQ 可使吸气爆发持续时间减少约 35%。这些来自减少准备的数据表明 preBötC 神经元中的 KCNQ 电流有助于吸气爆发终止。
The pre-Bötzinger complex (preBötC) of the ventral medulla generates the mammalian inspiratory breathing rhythm. When isolated in explants and deprived of synaptic inhibition, the preBötC continues to generate inspiratory-related rhythm. Mechanisms underlying burst generation have been investigated for decades, but cellular and synaptic mechanisms responsible for burst termination have received less attention. KCNQ-mediated K+ currents contribute to burst termination in other systems, and their transcripts are expressed in preBötC neurons. Therefore, we tested the hypothesis that KCNQ channels also contribute to burst termination in the preBötC. We recorded KCNQ-like currents in preBötC inspiratory neurons in neonatal rat slices that retain respiratory rhythmicity. Blocking KCNQ channels with XE991 or linopirdine (applied via superfusion or locally) increased inspiratory burst duration by 2- to 3-fold. By contrast, activation of KCNQ with retigabine decreased inspiratory burst duration by ~35%. These data from reduced preparations suggest that the KCNQ current in preBötC neurons contributes to inspiratory burst termination.
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