首页> 外文期刊>The Journal of Physiology >Slow excitatory synaptic potentials evoked by distension in myenteric descending interneurones of guinea-pig ileum.
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Slow excitatory synaptic potentials evoked by distension in myenteric descending interneurones of guinea-pig ileum.

机译:豚鼠回肠的肌间降神经元中的膨胀引起的缓慢的兴奋性突触电位。

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The functional significance of the slow excitatory synaptic potentials (EPSPs) in myenteric neurones is unknown. We investigated this using intracellular recording from myenteric neurones in guinea-pig ileum, in vitro. In all, 121 neurones responded with fast EPSPs to distension of the intestine oral to the recording site. In 28 of these neurones, distension also evoked depolarizations similar to the slow EPSPs evoked by electrical stimulation in the same neurones. Intracellular injection of biocytin and immunohistochemistry revealed that neurones responding to distension with slow EPSPs were descending interneurones, which were immunoreactive for nitric oxide synthase (NOS). Other neurones, including inhibitory motor neurones and interneurones lacking NOS, did not respond to distension with slow EPSPs, but many had slow EPSPs evoked electrically. Slow EPSPs evoked electrically or by distension in NOS-immunoreactive descending interneurones were resistant to blockade of NK(1) or NK(3) tachykinin receptors (SR 140333, 100 nM; SR 142801, 100 nM, respectively) and group I metabotropic glutamate receptors (PHCCC, 10-30 microM), when the antagonists were applied in the recording chamber of a two-chambered organ bath. However, slow EPSPs evoked electrically in inhibitory motor neurones were substantially depressed by SR 140333 (100 nM). Blockade of synaptic transmission in the stimulation chamber of the organ bath abolished slow EPSPs evoked by distension, indicating that they arose from activity in interneurones, and not from anally directed, intrinsic sensory neurones. Thus, distension evokes slow EPSPs in a subset of myenteric neurones, which may be important for intestinal motility.
机译:肌层神经元中缓慢的兴奋性突触电位(EPSP)的功能意义尚不清楚。我们调查了使用豚鼠回肠肌层神经元的细胞内记录进行体外研究。总之,有121个神经元对快速EPSP响应了记录部位的肠道扩张。在这些神经元中的28个中,与相同神经元中的电刺激诱发的缓慢EPSP相似,扩张也引起了去极化。胞内注射生物素和免疫组化显示,对缓慢扩张的EPSP的扩张反应的神经元是降级间质,对一氧化氮合酶(NOS)具有免疫反应性。其他神经元,包括抑制性运动神经元和缺乏NOS的中间神经元,对缓慢的EPSP不会对扩张产生反应,但许多神经元具有电诱发的缓慢的EPSP。在NOS免疫反应性下降的中间神经元中通过电动或扩张引起的慢速EPSP对NK(1)或NK(3)速激肽受体(分别为SR 140333、100 nM,SR 142801、100 nM)和I组代谢型谷氨酸受体的阻滞具有抗性(PHCCC,10-30 microM),当拮抗剂在两腔器官浴的记录室中使用时。但是,SR 140333(100 nM)基本上抑制了抑制性运动神经元中电诱发的慢速EPSP。器官浴刺激腔中突触传递的阻滞消除了由扩张引起的慢速EPSP,这表明它们起因于中间神经元的活动,而不是由肛门定向的内在感觉神经元引起。因此,膨胀引起了一部分肌层神经元的慢速EPSP,这可能对肠道运动很重要。

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