Norepinephrine Restores Inhibitory Tone of Spinal Lamina X Circuitry, thus Contributing to Analgesia Against Inflammatory Pain
Norepinephrine Restores Inhibitory Tone of Spinal Lamina X Circuitry, thus Contributing to Analgesia Against Inflammatory Pain
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去甲肾上腺素可恢复椎板 X 回路的抑制张力，从而有助于镇痛对抗炎性疼痛
DOI：
10.1016/j.neuroscience.2022.03.023
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发表时间：
2022
期刊：
影响因子：
3.3
通讯作者：
Hiroshi Baba
中科院分区：
文献类型：
--
作者：
Nobuko Ohashi;Daisuke Uta;Masayuki Ohashi;Hiroshi Baba
去甲肾上腺素（NE）直接作用于脊髓X板层的抑制性中间神经元，并可作用于脊髓X板层神经元以抑制对抗疼痛的伤害性突触传递。我们在炎症性疼痛模型大鼠中研究了这一机制。免疫组化染色和在体细胞外记录显示，NE可明显抑制炎性疼痛时X板层磷酸化细胞外信号调节激酶（ERK）的增加（n= 6/组）和X板层自发放电频率的增加（n= 14）（P< 0.01）。在体内观察增强的自发神经元放电后，我们使用体外脊髓切片制备来测试NE对这种放电的影响。用膜片钳技术记录脊髓X板层神经元上的微小抑制性突触后电流（miniature inhibitory postsynaptic currents，mIPSCs）频率在炎症痛时降低。在炎症性疼痛模型大鼠中，直接将NE应用于脊髓X板神经元可增加mIPSC的频率并诱导外向电流（n= 8;P< 0.05），这些反应可被α1A和α2受体拮抗剂抑制（n= 8;P> 0.05）。考虑到这些结果和我们以前的研究（Ohashi等人，2019），NE可能作用于脊髓X层的抑制性中间神经元，以促进抑制性传递并诱导位于X层膜内或周围的神经元超极化。这些NE介导的反应通过α1A-和α2-受体起作用。NE在脊髓X板层的这些作用机制可能有助于减轻炎性痛。
Norepinephrine (NE) acts directly on the inhibitory interneurons of spinal lamina X and may act on spinal lamina X neurons for inhibiting nociceptive synaptic transmission against pain. We investigated this mechanism within inflammatory pain model rats. Using immunohistochemical staining andin vivoextracellular recording, the increased number of phosphorylated extracellular signal-regulated kinase profiles in lamina X (n= 6/group) and increased frequency of spontaneous neuronal firing on putative lamina X (n= 14) under the inflammatory pain were significantly suppressed by the direct application of NE (P< 0.01). Followingin vivoobservation of enhanced spontaneous neuronal firing, we tested the impact of NE on this discharge using anin vitrospinal slice preparation. Usingin vitropatch-clamps recording, the baseline level of miniature inhibitory postsynaptic currents (mIPSCs) frequency on spinal lamina X neurons cord is decreased under inflammatory pain. Direct application of NE to spinal lamina X neurons in inflammatory pain model rats facilitates mIPSCs frequency and induces an outward current (n= 8;P< 0.05), and these responses are inhibited by α1A- and α2-receptor antagonists (n= 8;P> 0.05). Considering these results and those of our previous study (Ohashi et al., 2019), NE might act on inhibitory interneurons of spinal lamina X to facilitate inhibitory transmission and induces neurons located in or around lamina X membrane hyperpolarization. These NE-mediated responses acted through α1A- and α2-receptors. These mechanisms of NE on spinal lamina X might contribute to analgesia against inflammatory pain.
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影响因子：
4.6
作者：
Ohashi N;Sasaki M;Ohashi M;Kamiya Y;Baba H;Kohno T
通讯作者：
Kohno T
影响因子：
2.5
作者：
BENNETT, GJ;ABDELMOUMENE, M;DUBNER, R
通讯作者：
DUBNER, R
影响因子：
2.5
作者：
KOEKKOEK, SKE;RUIGROK, TJH
通讯作者：
RUIGROK, TJH
新生大鼠脊髓X层GABA/甘氨酸的共释放
影响因子：
1.7
作者：
Riad Seddik;R. Schlichter;J. Trouslard
通讯作者：
J. Trouslard
DOI：
--
发表时间：
1995-10
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
D. M. Dirig;Tony L. Yaksh
通讯作者：
D. M. Dirig;Tony L. Yaksh