脊髓 μ 和 δ 阿片受体抑制大鼠的热痛和机械痛。
Spinal μ and δ opioids inhibit both thermal and mechanical pain in rats.
机构信息
Département de physiologie et biophysique, Faculté de médecine et des sciences de la santé, Institut de pharmacologie de Sherbrooke, and Centre de recherche clinique Étienne-Le Bel, Université de Sherbrooke, Sherbrooke, QC, Canada.
出版信息
J Neurosci. 2013 Jul 10;33(28):11703-14. doi: 10.1523/JNEUROSCI.1631-13.2013.
The expression and contribution of μ (MOPR) and δ opioid receptors (DOPR) in polymodal nociceptors have been recently challenged. Indeed, MOPR and DOPR were shown to be expressed in distinct subpopulation of nociceptors where they inhibit pain induced by noxious heat and mechanical stimuli, respectively. In the present study, we used electrophysiological measurements to assess the effect of spinal MOPR and DOPR activation on heat-induced and mechanically induced diffuse noxious inhibitory controls (DNICs). We recorded from wide dynamic range neurons in the spinal trigeminal nucleus of anesthetized rats. Trains of 105 electrical shocks were delivered to the excitatory cutaneous receptive field. DNICs were triggered either by immersion of the hindpaw in 49°C water or application of 300 g of mechanical pressure. To study the involvement of peptidergic primary afferents in the activation of DNIC by noxious heat and mechanical stimulations, substance P release was measured in the spinal cord by visualizing neurokinin type 1 receptor internalization. We found that the activation of spinal MOPR and DOPR similarly attenuates the DNIC and neurokinin type 1 receptor internalization induced either by heat or mechanical stimuli. Our results therefore reveal that the activation of spinal MOPR and DOPR relieves both heat-induced and mechanically induced pain with similar potency and suggest that these receptors are expressed on polymodal, substance P-expressing neurons.
μ(MOPR)和 δ 阿片受体(DOPR)在多模式伤害感受器中的表达和贡献最近受到了挑战。事实上,MOPR 和 DOPR 被证明在伤害感受器的不同亚群中表达,它们分别抑制有害热和机械刺激引起的疼痛。在本研究中,我们使用电生理测量来评估脊髓 MOPR 和 DOPR 激活对热诱导和机械诱导的弥散性伤害性抑制控制(DNIC)的影响。我们记录了麻醉大鼠三叉神经脊束核中宽动态范围神经元的活动。用 105 个电脉冲的序列刺激兴奋性皮肤感受野。通过将后足浸入 49°C 水中或施加 300g 的机械压力来触发 DNIC。为了研究伤害性热和机械刺激激活 DNIC 中肽能初级传入纤维的参与,通过可视化神经激肽 1 型受体内化来测量脊髓中的神经激肽释放。我们发现,脊髓 MOPR 和 DOPR 的激活同样减弱了由热或机械刺激引起的 DNIC 和神经激肽 1 型受体内化。因此,我们的结果表明,脊髓 MOPR 和 DOPR 的激活以相似的效力缓解热诱导和机械诱导的疼痛,并表明这些受体表达在多模式、神经激肽表达神经元上。