Neuropharmacological study on integration and modulation of synaptic inputs in the central rhythm generation network

为了研究中枢节律发生网络中突触输入的整合和调制，记录了去大脑、未麻醉、切断迷走神经、人工通气猫延髓呼吸神经元的膜电位、动作电位和突触后电位。得到以下结果.来自肺传入神经和脑桥呼吸调节中心（臂旁内侧核：NPBM）的突触输入通过不同的途径在中枢呼吸神经元上传递，但以类似的方式传递。这些输入由NMDA受体机制调节。特别是，NMDA机制被认为是增强和/或同步晚I神经元的吸气末去极化和放电，导致GABA释放，从而关闭延髓吸气神经元和膈运动神经元的开关。因此，NMDA介导的后I和后I神经元的顺序去极化在IOS中起着至关重要的作用。在阻断NMDA受体诱发的呼吸暂停过程中，IOS是由非NMDA介导的late-I和post-I神经元的快速兴奋引起的，随后是aug-E神经元的兴奋.呼吸神经元通过细胞内记录膜电位和用神经生物素进行细胞内标记来鉴定。免疫荧光双标法检测谷氨酸脱羧酶和NMDA受体的分布。所有类型的固有延髓呼吸神经元都是GABA能神经元。NMDA受体在球脊髓aug-E神经元中的分布较其他类型神经元少.来源于ryanodine敏感性Ca^2+库的Ca^2+通过激活Ca^2+依赖性K^+通道来调节呼吸神经元中突触诱导的周期性膜电位波动和爆发活动。

To investigate integration and modulation of synaptic inputs in the central rhythm generation network, membrane potential, action potential and postsynaptic potentials were recorded from bulbar respiratory neurons in decerebrate, unanesthetized, vagotomized, artificially ventilated cats. The following results were obtained.1. Synaptic inputs from the pulmonary afferents and the pontine pneumotaxic center (nucleus parabrachialis medialis : NPBM) were conveyed on the central respiratory neurons through different pathways but transmitted in a similar manner. These inputs were modulated by NMDA receptor mechanisms. Especially, the NMDA mechanisms are assumed to augment and/or synchronize the late-inspiratory depolarization and discharge of late-I neurons, leading to GABA release and consequently off-switching of bulbar inspiratory neurons and phrenic motoneurons. Therefore, the NMDA-mediated sequential depolarization of late-I and post-I neurons plays an essential role in IOS. During apneusis evoked by blockade of NMDA receptors, IOS was induced by non-NMDA-mediated rapid excitation of late-I and post-I neurons, which was followed by excitation of aug-E neurons.2. Respiratory neurons were identified by intracellular recording of membrane potential and by intracellular labeling with neurobiotin. These neurons were examined distribution of glutamic acid decarboxylase or NMDA receptors by double immunofluorescent staining. All types of propriobulbar respiratory neurons are GABAergic. NMDA receptors are distributed in lesser degree in bulbospinal aug-E neurons than in other types of neurons.3. Ca^<2+> derived from ryanodine-sensitive Ca^<2+> stores modulates the synaptically induced periodic membrane potential fluctuations and burst activity in respiratory neurons through activating the Ca^<2+>-dependent K^+ channels.