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猫NMDA受体阻断后诱发相位转换期间呼吸神经元的突触电位

Synaptic potentials in respiratory neurones during evoked phase switching after NMDA receptor blockade in the cat.

作者信息

Pierrefiche O, Haji A, Foutz A S, Takeda R, Champagnat J, Denavit-Saubie M

机构信息

Physiologie Animale, Faculte des Sciences, Universite de Picardie Jules Verne, 80039 Amiens, France.

出版信息

J Physiol. 1998 Apr 15;508 ( Pt 2)(Pt 2):549-59. doi: 10.1111/j.1469-7793.1998.549bq.x.

Abstract
  1. Blockade of NMDA receptors by dizocilpine impairs the inspiratory off-switch (IOS) of central origin but not the IOS evoked by stimulation of sensory afferents. To investigate whether this difference was due to the effects of different patterns of synaptic interactions on respiratory neurones, we stimulated electrically the superior laryngeal nerve (SLN) or vagus nerve in decerebrate cats before and after i.v. administration of dizocilpine, whilst recording intracellularly. 2. Phrenic nerve responses to ipsilateral SLN or vagal stimulation were: at mid-inspiration, a transient inhibition often followed by a brief burst of activity; at late inspiration, an IOS; and at mid-expiration, a late burst of activity. 3. In all neurones (n = 16), SLN stimulation at mid-inspiration evoked an early EPSP during phase 1 (latency to the arrest of phrenic nerve activity), followed by an IPSP in inspiratory (I) neurones (n = 8) and by a wave of EPSPs in post-inspiratory (PI) neurones (n = 8) during phase 2 (inhibition of phrenic activity). An EPSP in I neurones and an IPSP in PI neurones occurred during phase 3 (brief phrenic burst) following phase 2. 4. Evoked IOS was associated with a fast (phase 1) activation of PI neurones, whereas during spontaneous IOS, a progressive (30-50 ms) depolarization of PI neurones preceded the arrest of phrenic activity. 5. Phase 3 PSPs were similar to those occurring during the burst of activity seen at the start of spontaneous inspiration. 6. Dizocilpine did not suppress the evoked phrenic inhibition and the late burst of activity. The shapes and timing of the evoked PSPs and the changes in membrane potential in I and PI neurones during the phase transition were not altered. 7. We hypothesize that afferent sensory pathways not requiring NMDA receptors (1) terminate inspiration through a premature activation of PI neurones, and (2) evoke a late burst of phrenic activity which might be the first stage of the inspiratory on-switch.
摘要
  1. 地卓西平对N-甲基-D-天冬氨酸(NMDA)受体的阻断作用会损害中枢起源的吸气切断机制(IOS),但不会影响由感觉传入神经刺激诱发的IOS。为了研究这种差异是否是由于不同模式的突触相互作用对呼吸神经元的影响所致,我们在静脉注射地卓西平前后,对去大脑猫的喉上神经(SLN)或迷走神经进行电刺激,同时进行细胞内记录。2. 膈神经对同侧SLN或迷走神经刺激的反应如下:在吸气中期,先是短暂抑制,随后常伴有短暂的活动爆发;在吸气后期,出现IOS;在呼气中期,出现后期活动爆发。3. 在所有神经元(n = 16)中,吸气中期刺激SLN在第1阶段(膈神经活动停止的潜伏期)诱发早期兴奋性突触后电位(EPSP),随后在吸气(I)神经元(n = 8)中出现抑制性突触后电位(IPSP),在吸气后(PI)神经元(n = 8)的第2阶段(膈神经活动抑制)出现一波EPSP。在第2阶段后的第3阶段(短暂的膈神经爆发),I神经元出现EPSP,PI神经元出现IPSP。4. 诱发的IOS与PI神经元的快速(第1阶段)激活相关,而在自发的IOS期间,PI神经元先出现逐渐(30 - 50毫秒)的去极化,然后膈神经活动停止。5. 第3阶段的突触后电位(PSP)与自发吸气开始时活动爆发期间出现的PSP相似。6. 地卓西平并未抑制诱发的膈神经抑制和后期活动爆发。诱发的PSP的形状和时间以及I和PI神经元在阶段转换期间膜电位的变化均未改变。7. 我们推测,不需要NMDA受体的传入感觉通路(1)通过PI神经元的过早激活终止吸气,(2)诱发膈神经活动的后期爆发,这可能是吸气开启机制的第一阶段。

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