Sciatic nerve stimulation activates the retrotrapezoid nucleus in anesthetized rats.
Sciatic nerve stimulation activates the retrotrapezoid nucleus in anesthetized rats.
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坐骨神经刺激激活麻醉大鼠的后梯形核。
DOI：
10.1152/jn.00543.2016
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发表时间：
2016
影响因子：
2.5
通讯作者：
Guyenet,PatriceG
中科院分区：
文献类型：
--
作者：
Kanbar,Roy;Stornetta,RuthL;Guyenet,PatriceG
后斜方核（RTN）神经元维持呼吸自律性。这些神经元具有化学感受器特性，但它们的放电也受到功能不确定的多个突触输入的调节。在这里，我们测试是否RTN神经元，像邻近的前交感神经元，兴奋的躯体传入刺激。实验在Inactin麻醉、双侧迷走神经切断、麻痹、机械通气的Sprague-Dawley大鼠中进行。呼气末CO2（eeCO 2）在4%和10%之间变化，以改变膈神经放电（PND）的速率和幅度。RTN和前交感神经元被记录在面运动核下方的细胞外。坐骨神经刺激（SNstim，1 ms，0.5 Hz）轻微增加血压（6.6 ± 1.6 mmHg）和心率，并在低eeCO 2（<5.5%）时引起PND。同侧和对侧SNstim产生了已知的前交感神经元的双相激活。SNstim在高达67%的RTN神经元中引起类似但较弱的双相反应，在其余神经元中引起单相兴奋。在低eeCO 2，RTN神经元沉默，更弱的SNstim比在高eeCO 2。RTN神经元放电受到不同程度的呼吸调制。在高eeCO 2时，当PND对刺激的夹带被破坏时，SNstim引起的RTN神经元的阶段性激活几乎没有变化。因此，RTN神经元对SNstim的反应不是由对中央模式发生器的夹带引起的。总的来说，SNstim向上移动了RTN点火和eeCO 2之间的关系。结论：躯体传入刺激增加了RTN神经元放电概率，但不改变其对CO2的反应，这一通路可能与伤害性感受、运动（肌肉代谢反射）或体温过高引起的呼吸过度有关。
Retrotrapezoid nucleus (RTN) neurons sustain breathing automaticity. These neurons have chemoreceptor properties, but their firing is also regulated by multiple synaptic inputs of uncertain function. Here we test whether RTN neurons, like neighboring presympathetic neurons, are excited by somatic afferent stimulation. Experiments were performed in Inactin-anesthetized, bilaterally vagotomized, paralyzed, mechanically ventilated Sprague-Dawley rats. End-expiratory CO2(eeCO2) was varied between 4% and 10% to modify rate and amplitude of phrenic nerve discharge (PND). RTN and presympathetic neurons were recorded extracellularly below the facial motor nucleus with established criteria. Sciatic nerve stimulation (SNstim, 1 ms, 0.5 Hz) slightly increased blood pressure (6.6 ± 1.6 mmHg) and heart rate and, at low eeCO2(<5.5%), entrained PND. Ipsi- and contralateral SNstim produced the known biphasic activation of presympathetic neurons. SNstim evoked a similar but weaker biphasic response in up to 67% of RTN neurons and monophasic excitation in the rest. At low eeCO2,RTN neurons were silent and responded more weakly to SNstim than at high eeCO2. RTN neuron firing was respiratory modulated to various degrees. The phasic activation of RTN neurons elicited by SNstim was virtually unchanged at high eeCO2when PND entrainment to the stimulus was disrupted. Thus RTN neuron response to SNstim did not result from entrainment to the central pattern generator. Overall, SNstim shifted the relationship between RTN firing and eeCO2upward. In conclusion, somatic afferent stimulation increases RTN neuron firing probability without altering their response to CO2.This pathway may contribute to the hyperpnea triggered by nociception, exercise (muscle metabotropic reflex), or hyperthermia.