Shanghai Clinical Research Center, Chinese Academy of Sciences/XuHui Central Hospital, Shanghai, 200031, China.
Institute of Neuroscience and State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science, Chinese Academy of Sciences, Shanghai, 200031, China.
Sci China Life Sci. 2017 Sep;60(9):1013-1018. doi: 10.1007/s11427-017-9061-y. Epub 2017 Jun 15.
Noxious stimuli cause pain by activating cutaneous nociceptors. The Aδ- and C-fibers of dorsal root ganglion (DRG) neurons convey the nociceptive signals to the laminae I-II of spinal cord. In the dorsal horn of spinal cord, the excitatory afferent synaptic transmission is regulated by the inhibitory neurotransmitter γ-aminobutyric acid and modulators such as opioid peptides released from the spinal interneurons, and by serotonin, norepinepherine and dopamine from the descending inhibitory system. In contrast to the accumulated evidence for these central inhibitors and their neural circuits in the dorsal spinal cord, the knowledge about the endogenous suppressive mechanisms in nociceptive DRG neurons remains very limited. In this review, we summarize our recent findings of the presynaptic suppressive mechanisms in nociceptive neurons, the BNP/NPR-A/PKG/BKCa channel pathway, the FSTL1/α1Na-K ATPase pathway and the activin C/ERK pathway. These endogenous suppressive systems in the mechanoheat nociceptors may also contribute differentially to the mechanisms of nerve injury-induced neuropathic pain or inflammation-induced pain.
有害刺激通过激活皮肤伤害感受器引起疼痛。背根神经节（DRG）神经元的 Aδ 和 C 纤维将伤害性信号传递到脊髓的 I-II 层。在脊髓背角，兴奋性传入突触传递受来自脊髓中间神经元的抑制性神经递质 γ-氨基丁酸和阿片肽等调节剂以及来自下行抑制系统的 5-羟色胺、去甲肾上腺素和多巴胺的调节。与这些中枢抑制剂及其在脊髓背侧的神经回路的累积证据相比，关于伤害性 DRG 神经元中内源性抑制机制的知识仍然非常有限。在这篇综述中，我们总结了我们最近关于伤害性神经元中突触前抑制机制的发现，即 BNP/NPR-A/PKG/BKCa 通道途径、FSTL1/α1Na-K ATPase 途径和 activin C/ERK 途径。机械热伤害感受器中的这些内源性抑制系统也可能对神经损伤引起的神经性疼痛或炎症引起的疼痛的机制产生不同的影响。
