Department of Molecular Pharmacology and Physiology, College of Medicine, University of South Florida, Tampa, Florida 33612-4799, USA.
J Neurophysiol. 2012 Jan;107(2):603-17. doi: 10.1152/jn.00808.2011. Epub 2011 Oct 12.
Ventrolateral respiratory column (VRC) circuits that modulate breathing in response to changes in central chemoreceptor drive are incompletely understood. We employed multielectrode arrays and spike train correlation methods to test predictions of the hypothesis that pre-Bötzinger complex (pre-BötC) and retrotrapezoid nucleus/parafacial (RTN-pF) circuits cooperate in chemoreceptor-evoked tuning of ventral respiratory group (VRG) inspiratory neurons. Central chemoreceptors were selectively stimulated by injections of CO(2)-saturated saline into the vertebral artery in seven decerebrate, vagotomized, neuromuscularly blocked, and artificially ventilated cats. Among sampled neurons in the Bötzinger complex (BötC)-to-VRG region, 70% (161 of 231) had a significant change in firing rate after chemoreceptor stimulation, as did 70% (101 of 144) of the RTN-pF neurons. Other responsive neurons (24 BötC-VRG; 11 RTN-pF) had a change in the depth of respiratory modulation without a significant change in average firing rate. Seventy BötC-VRG chemoresponsive neurons triggered 189 offset-feature correlograms (96 peaks; 93 troughs) with at least one responsive BötC-VRG cell. Functional input from at least one RTN-pF cell could be inferred for 45 BötC-VRG neurons (19%). Eleven RTN-pF cells were correlated with more than one BötC-VRG target neuron, providing evidence for divergent connectivity. Thirty-seven RTN-pF neurons, 24 of which were chemoresponsive, were correlated with at least one chemoresponsive BötC-VRG neuron. Correlation linkage maps and spike-triggered averages of phrenic nerve signals suggest transmission of chemoreceptor drive via a multipath network architecture: RTN-pF modulation of pre-BötC-VRG rostral-to-caudal excitatory inspiratory neuron chains is tuned by feedforward and recurrent inhibition from other inspiratory neurons and from "tonic" expiratory neurons.
腹外侧呼吸柱 (VRC) 回路通过调节中央化学感受器驱动来调节呼吸,但目前对此了解甚少。我们采用多电极阵列和尖峰序列相关方法,测试了前 Bötzinger 复合体 (pre-BötC) 和延髓呼吸核/副核(parafacial, RTN-pF) 回路在化学感受器诱发的腹侧呼吸群 (ventral respiratory group, VRG) 吸气神经元调谐中合作的假设。在七只去大脑、迷走神经切断、神经肌肉阻断和人工通气的猫中,通过向椎动脉注入 CO2 饱和盐水来选择性刺激中枢化学感受器。在 Bötzinger 复合体 (BötC) 到 VRG 区域中,70%(231 个中的 161 个)的神经元在化学感受器刺激后放电率有显著变化,RTN-pF 神经元中也有 70%(144 个中的 101 个)的神经元有显著变化。其他反应性神经元(24 个 BötC-VRG;11 个 RTN-pF)的呼吸调制深度发生变化,但平均放电率无显著变化。70 个 BötC-VRG 化学感受器反应性神经元触发了 189 个偏移特征相关图(96 个峰;93 个谷),其中至少有一个反应性 BötC-VRG 细胞。至少有一个 RTN-pF 细胞的功能输入可以推断出 45 个 BötC-VRG 神经元(19%)。11 个 RTN-pF 细胞与多个 BötC-VRG 靶神经元相关,这提供了发散性连接的证据。37 个 RTN-pF 神经元,其中 24 个是化学感受器反应性的,与至少一个化学感受器反应性 BötC-VRG 神经元相关。相关链接映射和膈神经信号的尖峰触发平均表明,化学感受器驱动通过多路径网络结构进行传递:RTN-pF 对 pre-BötC-VRG 头侧至尾侧兴奋性吸气神经元链的调制是由其他吸气神经元和“紧张”呼气神经元的前馈和回授抑制来调节的。