Interaction between the retrotrapezoid nucleus and the parafacial respiratory group to regulate active expiration and sympathetic activity in rats.
Interaction between the retrotrapezoid nucleus and the parafacial respiratory group to regulate active expiration and sympathetic activity in rats.
复制标题
梯形后核与面旁呼吸组之间的相互作用调节大鼠主动呼气和交感神经活动。
DOI：
10.1152/ajplung.00011.2018
复制
发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Takakura,AnaC
中科院分区：
文献类型：
--
作者：
Zoccal,DanielB;Silva,JosianeN;Barnett,WilliamH;Lemes,EduardoV;Falquetto,Barbara;Colombari,Eduardo;Molkov,YaroslavI;Moreira,ThiagoS;Takakura,AnaC
后斜方核（RTN）含有化学敏感细胞，将CO2依赖性兴奋性驱动分配给呼吸网络。这种驱动有助于呼吸中枢模式发生器（rCPG）的功能，并增加交感神经活动。还证明了在高碳酸血症期间，面旁呼吸组（pFRG）中的呼气晚期（晚期E）振荡器被激活并决定主动呼气的出现。然而，它仍然不清楚的微电路负责的兴奋性信号的分布的pFRG和rCPG在高CO2的条件下。在此，我们假设来自RTN中的化学敏感神经元的兴奋性输入对于pFRG中的晚E神经元的激活是必要的。使用去脑原位大鼠制备，我们发现，神经激肽-1受体表达神经元的RTN区域与物质P-皂草素共轭物的病变抑制晚E活动在腹神经（AbNs）和交感神经（SNs）和衰减膈神经（PN）活动的增加引起的高碳酸血症。另一方面，在pFRG中注射犬尿烯酸（100 mM）消除了AbN和胸SN中的晚E活性，但在高碳酸血症期间没有改变PN反应。离子电渗注射逆行示踪剂到成年大鼠的pFRG显示标记的phox 2b表达神经元内的RTN。我们的研究结果得到了RTN和pFRG区域内化学敏感性和晚E群体的数学建模的支持，这两个区域是两个独立但相互作用的群体，在高碳酸血症期间pFRG晚E神经元的激活需要来自RTN神经元的多巴胺能输入，RTN神经元本质上检测CO2/pH的变化。
The retrotrapezoid nucleus (RTN) contains chemosensitive cells that distribute CO2-dependent excitatory drive to the respiratory network. This drive facilitates the function of the respiratory central pattern generator (rCPG) and increases sympathetic activity. It is also evidenced that during hypercapnia, the late-expiratory (late-E) oscillator in the parafacial respiratory group (pFRG) is activated and determines the emergence of active expiration. However, it remains unclear the microcircuitry responsible for the distribution of the excitatory signals to the pFRG and the rCPG in conditions of high CO2. Herein, we hypothesized that excitatory inputs from chemosensitive neurons in the RTN are necessary for the activation of late-E neurons in the pFRG. Using the decerebrated in situ rat preparation, we found that lesions of neurokinin-1 receptor-expressing neurons in the RTN region with substance P-saporin conjugate suppressed the late-E activity in abdominal nerves (AbNs) and sympathetic nerves (SNs) and attenuated the increase in phrenic nerve (PN) activity induced by hypercapnia. On the other hand, kynurenic acid (100 mM) injections in the pFRG eliminated the late-E activity in AbN and thoracic SN but did not modify PN response during hypercapnia. Iontophoretic injections of retrograde tracer into the pFRG of adult rats revealed labeled phox2b-expressing neurons within the RTN. Our findings are supported by mathematical modeling of chemosensitive and late-E populations within the RTN and pFRG regions as two separate but interacting populations in a way that the activation of the pFRG late-E neurons during hypercapnia require glutamatergic inputs from the RTN neurons that intrinsically detect changes in CO2/pH.