Activity of respiratory neurons during hypoxia in the chemodenervated cat.
Activity of respiratory neurons during hypoxia in the chemodenervated cat.
复制标题
化学去神经猫缺氧期间呼吸神经元的活动。
DOI：
10.1152/jappl.1995.78.3.856
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Duffin,J
中科院分区：
文献类型：
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作者：
England,SJ;Melton,JE;Douse,MA;Duffin,J
麻痹的、迷走神经切断、外周化学去神经的猫暴露在缺氧环境中会导致最初的抑郁症和随后的膈神经图丧失。为了确定缺氧呼吸抑制是否是由 Botzinger 复合体的球脊髓神经元（Bot-E 神经元）抑制呼吸前运动神经元引起的，在急性缺氧缺氧期间，对背侧和腹侧呼吸组球脊髓吸气神经元和 Bot-E 神经元进行了细胞外记录。所有神经元在缺氧期间记录放电率降低。 Bot-E 神经元在缺氧期间失去阶段性膈活动之前变得沉默，并在复氧期间膈神经图恢复之前或同时开始放电。吸气神经元停止放电与膈寂静同时发生。在常氧期间，相对于膈神经图，背侧呼吸组和腹侧呼吸组神经元的放电开始较晚，而在缺氧期间，吸气时放电逐渐提前，这种效应在复氧过程中被逆转。这些数据与作为缺氧呼吸抑制机制的抑制和/或阻碍一致，但表明 Bot-E 神经元不是这种抑制的根源。
Exposure of anesthetized paralyzed vagotomized peripherally chemodenervated cats to hypoxia results in initial depression and subsequent loss of the phrenic neurogram. To determine whether hypoxic respiratory depression results from the inhibition of respiratory premotor neurons by bulbospinal neurons of the Botzinger complex (Bot-E neurons), extracellular recordings were made of dorsal and ventral respiratory group bulbospinal inspiratory neurons and Bot-E neurons during acute hypoxic hypoxia. All neurons recorded decreased firing rate during hypoxia. Bot-E neurons became silent before the loss of phasic phrenic activity during hypoxia and commenced firing before or coincident with the return of the phrenic neurogram during reoxygenation. Inspiratory neurons ceased firing coincident with phrenic silence. Dorsal respiratory group and ventral respiratory group neurons that had a late onset of firing with respect to the phrenic neurogram during normoxia fired progressively earlier in inspiration during hypoxia, an effect that was reversed during reoxygenation. These data are consistent with inhibition and/or disfacilitation as the mechanism of hypoxic respiratory depression but suggest that Bot-E neurons are not the source of this inhibition.