Regulation of ventral surface chemoreceptors by the central respiratory pattern generator

Regulation of ventral surface chemoreceptors by the central respiratory pattern generator
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DOI:
10.1523/jneurosci.2415-05.2005
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发表时间:
2005-09-28
影响因子:
5.3
通讯作者:
Bayliss, DA
Bayliss, DA
中科院分区:
医学1区
文献类型:
--
作者:
Guyenet, PG;Mulkey, DK;Bayliss, DA

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大鼠斜方体后核(RTN)含有神经元,这些神经元被描述为成人的中枢化学感受器和新生儿的呼吸节律起搏器[副面呼吸组(PfRG)]。在这里,我们测试了这样的假设,即rtn和pfRG神经元都是内在的化学敏感和强直放电神经元,其呼吸节律性是由来自中枢呼吸模式发生器(CPG)的突触反馈引起的。在氟烷麻醉的成人中,RTN神经元在4.5%呼气末(e-exp)二氧化碳以下保持沉默。它们的活性在3.2赫兹/1%二氧化碳浓度下呈线性增长,最高可达6.5%(CPG阈值),然后较慢地在10%二氧化碳浓度下以10赫兹的频率达到峰值。RTN神经元的呼吸调制在CPG阈值以下不存在,在CPG阈值之后逐渐增强,与pfRG神经元一样,典型的(42%)表现为靠近膈吸气的双周期活动减少。用犬尿酸(KYN)灭活CPG后,RTN神经元的放电与e-exp CO2(斜率,+1.7 Hz/1%CO2)和动脉pH(阈值,7.48;斜率,39 Hz/pH单位)呈线性关系。在出生后7-12天的冠状脑片上,RTN化学敏感神经元在pH值为7.55时不表达。它们的活性随着酸化到pH 7.2(35℃时为17 Hz/pH单位)而线性增加,并始终是紧张性的。综上所述,与其假设的中枢化学感受器作用一致,rtn/pfRG神经元线性编码pH,并在体内(Kyn处理)和体外断开与其余呼吸中心的连接时以紧张性放电。在体内,RTN神经元接受作为反馈的呼吸同步抑制输入,并将其特有的呼吸调制传递给这些神经元。
The rat retrotrapezoid nucleus (RTN) contains neurons described as central chemoreceptors in the adult and respiratory rhythm-generating pacemakers in neonates [parafacial respiratory group (pfRG)]. Here we test the hypothesis that both RTN and pfRG neurons are intrinsically chemosensitive and tonically firing neurons whose respiratory rhythmicity is caused by a synaptic feedback from the central respiratory pattern generator (CPG). In halothane- anesthetized adults, RTN neurons were silent below 4.5% end-expiratory (e-exp) CO2. Their activity increased linearly (3.2 Hz/1% CO2) up to 6.5% (CPG threshold) and then more slowly to peak similar to 10 Hz at 10% CO2. Respiratory modulation of RTN neurons was absent below CPG threshold, gradually stronger beyond, and, like pfRG neurons, typically (42%) characterized by twin periods of reduced activity near phrenic inspiration. After CPG inactivation with kynurenate (KYN), RTN neurons discharged linearly as a function of e-exp CO2 (slope, +1.7 Hz/1% CO2) and arterial pH (threshold, 7.48; slope, 39 Hz/pH unit). In coronal brain slices (postnatal days 7-12), RTN chemosensitive neurons were silent at pH 7.55. Their activity increased linearly with acidification up to pH 7.2 (17 Hz/pH unit at 35 degrees C) and was always tonic.In conclusion, consistent with their postulated central chemoreceptor role, RTN/ pfRG neurons encode pH linearly and discharge tonically when disconnected from the rest of the respiratory centers in vivo (KYN treatment) and in vitro. In vivo, RTN neurons receive respiratory synchronous inhibitory inputs that may serve as feedback and impart these neurons with their characteristic respiratory modulation.