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首页> 外文期刊>The European Journal of Neuroscience >Neurotensin inhibits background K+ channels and facilitates glutamatergic transmission in rat spinal cord dorsal horn.
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Neurotensin inhibits background K+ channels and facilitates glutamatergic transmission in rat spinal cord dorsal horn.

机译：神经降压素抑制背景K +通道并促进大鼠脊髓背角的谷氨酸能传递。

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摘要

Neurotensin (NT) is a neuropeptide involved in the modulation of nociception. We have investigated the actions of NT on cultured postnatal rat spinal cord dorsal horn (DH) neurons. NT induced an inward current associated with a decrease in membrane conductance in 46% of the neurons and increased the frequency of glutamatergic miniature excitatory synaptic currents in 37% of the neurons. Similar effects were observed in acute slices. Both effects of NT were reproduced by the selective NTS1 agonist JMV449 and blocked by the NTS1 antagonist SR48692 and the NTS1/NTS2 antagonist SR142948A. The NTS2 agonist levocabastine had no effect. The actions of NT persisted after inactivation of G(i/o) proteins by pertussis toxin but were absent after inactivation of protein kinase C (PKC) by chelerythrine or inhibition of the MAPK (ERK1/2) pathway by PD98059. Pre- and postsynaptic effects of NT were insensitive to classical voltage- and Ca(2+) -dependent K(+) channel blockers. The K(+) conductance inhibited by NT was blocked by Ba(2+) and displayed no or little inward rectification, despite the presence of strongly rectifying Ba(2+) -sensitive K(+) conductance in these neurons. This suggested that NT blocked two-pore domain (K2P) background K(+) -channels rather than inwardly rectifying K(+) channels. Zn(2+) ions, which inhibit TRESK and TASK-3 K2P channels, decreased NT-induced current. Our results indicate that in DH neurons NT activates NTS1 receptors which, via the PKC-dependent activation of the MAPK (ERK1/2) pathway, depolarize the postsynaptic neuron and increase the synaptic release of glutamate. These actions of NT might modulate the transfer and the integration of somatosensory information in the DH.
机译：神经降压素（NT）是一种参与伤害感受调节的神经肽。我们调查了NT对培养的产后大鼠脊髓背角（DH）神经元的作用。 NT诱导内向电流，与46％的神经元的膜电导降低相关，并在37％的神经元中增加谷氨酸能微型兴奋性突触电流的频率。在急性切片中观察到类似的效果。 NT的两种作用均由选择性NTS1激动剂JMV449再现，并被NTS1拮抗剂SR48692和NTS1 / NTS2拮抗剂SR142948A阻断。 NTS2激动剂左卡泊汀没有作用。百日咳毒素使G（i / o）蛋白失活后，NT的作用仍然存在，而白屈菜红碱使蛋白激酶C（PKC）失活或PD98059抑制MAPK（ERK1 / 2）途径后，NT的作用不存在。 NT的突触前和突触后效应对经典的电压和Ca（2+）依赖的K（+）通道阻滞剂不敏感。尽管这些神经元中存在强整流Ba（2+）敏感的K（+）电导，但NT抑制的K（+）电导被Ba（2+）阻滞并且显示没有或几​​乎没有向内整流。这表明NT阻止了两孔域（K2P）背景K（+）-通道，而不是向内整流K（+）通道。抑制TRESK和TASK-3 K2P通道的Zn（2+）离子降低了NT诱导的电流。我们的结果表明，在DH神经元中，NT激活NTS1受体，该受体通过PKC依赖的MAPK（ERK1 / 2）途径的激活，使突触后神经元去极化并增加谷氨酸的突触释放。 NT的这些动作可能会调节DH中体感信息的传递和整合。

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