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首页> 外文期刊>Journal of Neurophysiology >Characterization of biphasic modulation of spinal nociceptive transmission by neurotensin in the rat rostral ventromedial medulla.
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Characterization of biphasic modulation of spinal nociceptive transmission by neurotensin in the rat rostral ventromedial medulla.

机译：神经降压药在大鼠延髓腹侧延髓中对脊髓伤害感受性传递的双相调节的特征。

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摘要

Modulation of spinal nociceptive transmission by neurotensin microinjected in the rostral ventromedial medulla (RVM) was examined in anesthetized, paralyzed rats. Forty-three spinal dorsal horn neurons in the L3-L5 spinal segments responding to mechanical and noxious thermal stimulation (50 degrees C) of the plantar surface of the ipsilateral hind foot were studied. Spinal units were classified as either wide dynamic range or nociceptive specific and were located in spinal laminae I-V. Microinjection of neurotensin (0.03 pmol/0.2 microl) into the RVM produced a significant facilitation (135% of control) of spinal unit responses to noxious thermal stimulation (50 degrees C) that lasted approximately 12 min. In contrast, injection of greater doses of neurotensin (300 or 3,000 pmol) produced an inhibition of spinal unit responses to noxious heat (51.7 and 10.6% of control, respectively) that had a longer duration (60-120 min). The effects of neurotensin on wide-dynamic-range and nociceptive-specific neuron responses to noxious heat were qualitatively and quantitatively similar. Spinal unit responses to graded heating of the skin (42-50 degrees C) were completely inhibited after microinjection of 3,000 pmol of neurotensin into the RVM. Injection of a lesser dose of neurotensin (300 pmol), however, resulted in a partial inhibition of spinal unit responses and significantly reduced the slope of the stimulus-response function to graded heating of the skin. Transection of either the ipsilateral or contralateral dorsolateral funiculus (DLF) significantly reduced the inhibition of spinal nociceptive transmission produced by neurotensin (3,000 pmol) in the RVM, whereas bilateral transection of the DLFs completely blocked the effect. In contrast, bilateral transection of the DLFs had no effect on facilitation of spinal nociception by neurotensin (0.03 pmol) in the RVM. The inhibition of spinal nociceptive transmission by neurotensin (3,000 pmol) in the RVM was completely blocked by injection of the nonpeptide neurotensin receptor antagonist SR48692 (30 fmol) into the RVM 10 min before neurotensin. To confirm a specific block of neurotensin-receptor-mediated effects by the antagonist, a subsequent injection of L-glutamate into the RVM was performed. L-Glutamate (100 nmol) was found to inhibit the nociceptive responses of those spinal units whose responses were no longer inhibited by neurotensin. In contrast, injection of SR48692 (30 fmol) into the RVM failed to block the facilitation of spinal unit responses to noxious heat produced by a subsequent injection of neurotensin (0.03 pmol) into the same site. The present series of experiments demonstrate a specific role for neurotensin in the RVM in the modulation of spinal nociceptive transmission, because the peptide was found to both facilitate and inhibit spinal neuron responses to noxious thermal stimulation. Additionally, the facilitatory and inhibitory effects of neurotensin appear to occur via interaction with multiple neurotensin receptors in the RVM that activate independent systems that descend in the ventrolateral funiculi and DLFs, respectively. The results from these experiments are consistent with prior studies demonstrating that the RVM both facilitates and inhibits spinal nociceptive transmission, and they complement previous work showing that neurotensin in the RVM modulates spinal nociceptive behavioral responses.
机译：在麻醉的，瘫痪的大鼠中检查了微注射在延髓腹侧延髓（RVM）中的神经降压素对脊髓伤害感受性传递的调节。研究了L3-L5脊柱节段中的43个脊柱背角神经元，这些神经节对同侧后足的足底表面进行机械和有毒的热刺激（50摄氏度）。脊柱单位被分类为宽动态范围或伤害感受特异性，并位于脊柱I-V区。将神经降压素（0.03 pmol / 0.2微升）微量注射到RVM中，可显着促进（135％的对照）脊柱单位对有害热刺激（50摄氏度）的反应，持续约12分钟。相反，注射更大剂量的神经降压素（300或3,000 pmol）会抑制脊髓单位对有害热量的反应（分别为对照的51.7和10.6％），持续时间较长（60-120分钟）。神经降压素对宽动态范围和伤害性特异性神经元对有害热的反应在质量和数量上相似。将3,000 pmol神经降压素微注射到RVM中后，脊柱单位对皮肤逐渐升温（42-50摄氏度）的反应被完全抑制。但是，注射较少剂量的神经降压素（300 pmol）会导致部分抑制脊柱单位反应，并显着降低刺激反应功能对皮肤分级加热的斜率。横穿同侧或对侧背侧真菌（DLF）显着降低了RVM中神经降压素（3,000 pmol）产生的脊髓伤害性传递的抑制作用，而DLF的双侧横断完全阻断了该作用。相反，DLF的双侧横断对RVM中神经降压素（0.03 pmol）促进脊髓伤害感受没有作用。通过在神经降压素前10分钟向RVM中注射非肽神经降压素受体拮抗剂SR48692（30 fmol），可以完全阻止RVM中的神经降压素（3,000 pmol）抑制脊髓伤害性传递。为了确认拮抗剂能特异性阻断神经降压素受体介导的作用，随后将L-谷氨酸注射到RVM中。 L-谷氨酸（100 nmol）被发现可以抑制那些不再被神经降压素抑制的脊髓单元的伤害性反应。相反，向RVM注射SR48692（30 fmol）不能阻止脊柱单位对随后向同一部位注射神经降压素（0.03 pmol）产生的有害热量的反应。本系列实验证明了RVM中神经降压素在调节脊髓伤害性传递中的特定作用，因为发现该肽既促进和抑制了脊髓神经元对有害热刺激的反应。另外，神经降压素的促进作用和抑制作用似乎是通过与RVM中的多个神经降压素受体相互作用而发生的，该受体激活分别在腹外侧功能区和DLF中下降的独立系统。这些实验的结果与先前的研究一致，表明RVM既促进和抑制了脊髓伤害感受性传递，又补充了先前的工作，表明RVM中的神经降压素调节脊髓伤害感受行为响应。

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