Boadas-Vaello P, Castany S, Homs J, Álvarez-Pérez B, Deulofeu M, Verdú E
Research Group of Clinical Anatomy, Embryology and Neuroscience (NEOMA), Department of Medical Sciences, Universitat de Girona, Girona, Spain.
Department of Physical Therapy, EUSES - Universitat de Girona, Girona, Spain.
Spinal Cord. 2016 May;54(5):330-40. doi: 10.1038/sc.2015.225. Epub 2016 Jan 12.
This is a narrative review of the literature.
This review aims to be useful in identifying therapeutic targets. It focuses on the molecular and biochemical neuroplasticity changes that occur in the somatosensory system, including ascending and descending pathways, during the development of neuropathic pain. Furthermore, it highlights the latest experimental strategies, based on the changes reported in the damaged nociceptive neurons during neuropathic pain states.
This study was conducted in Girona, Catalonia, Spain.
A MEDLINE search was performed using the following terms: descending pain pathways; ascending pain pathways; central sensitization; molecular pain; and neuropathic pain pharmacological treatment.
Neuropathic pain triggered by traumatic lesions leads to sensitization and hyperexcitability of nociceptors and projection neurons of the dorsal horn, a strengthening in the descendent excitatory pathway and an inhibition of the descending inhibitory pathway of pain. These functional events are associated with molecular plastic changes such as overexpression of voltage-gated ion channels, algogen-sensitive receptors and synthesis of several neurotransmitters. Molecular studies on the plastic changes in the nociceptive somatosensory system enable the development of new pharmacological treatments against neuropathic pain, with higher specificity and effectiveness than classical drug treatments. Although research efforts have already focused on these aspects, additional research may be necessary to further explore the potential therapeutic targets in neuropathic pain involved in the neuroplasticity changes of neuropathological pathways from the injured somatosensory system.
这是一篇文献综述。
本综述旨在有助于确定治疗靶点。它聚焦于在神经性疼痛发展过程中,体感系统(包括上行和下行通路)中发生的分子和生化神经可塑性变化。此外,基于在神经性疼痛状态下受损伤害性神经元中报告的变化,突出了最新的实验策略。
本研究在西班牙加泰罗尼亚的赫罗纳进行。
使用以下术语在MEDLINE数据库中进行检索:下行疼痛通路;上行疼痛通路;中枢敏化;分子疼痛;以及神经性疼痛的药物治疗。
创伤性损伤引发的神经性疼痛会导致伤害感受器和背角投射神经元的敏化和兴奋性过高,下行兴奋性通路增强以及下行疼痛抑制通路受到抑制。这些功能事件与分子可塑性变化相关,如电压门控离子通道、促痛敏感受体的过度表达以及几种神经递质的合成。对伤害性体感系统可塑性变化的分子研究有助于开发针对神经性疼痛的新药,其特异性和有效性高于传统药物治疗。尽管研究工作已经聚焦于这些方面,但可能仍需要进一步研究,以进一步探索涉及来自受损体感系统神经病理通路神经可塑性变化的神经性疼痛潜在治疗靶点。