Phase switching of respiratory rhythm in bulbar respiratory neuronal network

为探讨呼吸节律产生的时相转变过程，在去大脑、未麻醉、去迷走神经、人工呼吸的猫上，记录了呼吸节律产生的吸气关断(LOS)和通电(ON)、膜电位和突触后电位。取得了以下研究成果：1.结论：1.真核呼吸发生在延髓呼吸神经元网络内，不存在肺传入和桥肺传入。在IOS中，对Late-I神经元和P1神经元的顺序兴奋抑制了Aug-I神经元的吸气活动。阻断NMDA受体通过破坏这一LOS机制而导致窒息。在停滞过程中，通过激活非NMDA受体来兴奋E2神经元，从而诱导IOS的产生。在IOS过程中，最终的抑制性传递到AUG-I神经元是由GABA-A受体机制介导的。迷走神经刺激诱导的IOS可在延髓呼吸神经元诱发短潜伏期突触后电位。这些突触后反应类似于迷走神经诱导的离子刺激。低阈值钙电流参与呼吸神经元从静止期向活跃期的反弹去极化。

To investigate the phase transitional process of respiratory rhythm generation, inspiratory off-switching (LOS) and on-switching (IonS), membrane potential and postsynaptic potentials were recorded from bulbar respiratory neurons in decerebrate, unanesthetized, vagotomized, artificially ventilated cats. The following results were obtained.1. Eupneic respiration was generated within the bulbar respiratory neuronal network without pulmonary afferent inputs and pontine pneumotaxic inputs.2. During IOS, a sequential excitation of late-I neurons and P1 neurons inhibited the inspiratory activity of aug-I neurons. Blockade of NMDA receptors resulted in apneusis by impairing this lOS mechanism. During apneusis, IOS was induced by excitation of E2 neurons through activation of non-NMDA receptors.3. During IOS, the final inhibitory transmission to aug-I neurons was mediated by the GABA-A receptor mechanism.4. Short latency postsynaptic potentials were evoked in bulbar respiratory neurons during IOS induced by vagal stimulation. These postsynaptic responses were similar to those during the vagally induced IonS.5. Low-threshold Ca currents involved in the rebound depolarization of respiratory neurons at the transitional phase from the inactive phase to the active phase.