疼痛是由外周伤害性输入和中枢加工的复杂整合引起的感觉状态。疼痛包括急性和有益于愈合的适应性疼痛和通常是持续和病理性的适应性不良疼痛。疼痛确实是异质的,可以表现为伤害性,炎症,或者本质上是神经性的。神经性疼痛是脊髓损伤(SCI)后发生的适应不良疼痛的一个例子。这引发了广泛的神经可塑性。在脊髓中充分研究了导致疼痛超敏反应的伤害性过程。然而,最近的调查显示,适应性不良的可塑性会导致疼痛,包括SCI后的神经性疼痛,也存在于外周部位,例如背根神经节(DRG),包含感觉神经元的细胞体。这篇综述讨论了DRGs在炎症和神经性疼痛基础上的伤害性处理中的重要作用。具体来说,它强调了痛觉感受器过度兴奋是增加疼痛状态的关键。此外,它回顾了先前关于谷氨酸和谷氨酸受体的文献,电压门控钠通道(VGSC),DRG中的脑源性神经营养因子(BDNF)信号是炎症和神经性疼痛的重要贡献者。我们先前回顾了BDNF作为脊柱可塑性的双向神经调质的作用。这里,我们将焦点转移到外围,并讨论BDNF-TrkB在伤害感受器上的表达,非痛觉感受器感觉神经元,和外周的非神经元细胞是SCI后疼痛诱导和持续的潜在贡献者。总的来说,这篇综述对单独关注疼痛的大型工作机构进行了全面评估,DRG,BDNF,和SCI,以了解它们在伤害性加工中的相互作用。
Pain is a sensory state resulting from complex integration of peripheral nociceptive inputs and central processing. Pain consists of adaptive pain that is acute and beneficial for healing and maladaptive pain that is often persistent and pathological. Pain is indeed heterogeneous, and can be expressed as nociceptive, inflammatory, or neuropathic in nature. Neuropathic pain is an example of maladaptive pain that occurs after spinal cord injury (SCI), which triggers a wide range of neural plasticity. The nociceptive processing that underlies pain hypersensitivity is well-studied in the spinal cord. However, recent investigations show maladaptive plasticity that leads to pain, including neuropathic pain after SCI, also exists at peripheral sites, such as the dorsal root ganglia (DRG), which contains the cell bodies of sensory neurons. This
review discusses the important role DRGs play in nociceptive processing that underlies inflammatory and neuropathic pain. Specifically, it highlights nociceptor hyperexcitability as critical to increased pain states. Furthermore, it reviews prior literature on glutamate and glutamate receptors, voltage-gated sodium channels (VGSC), and brain-derived neurotrophic factor (BDNF) signaling in the DRG as important contributors to inflammatory and neuropathic pain. We previously reviewed BDNF\'s role as a bidirectional neuromodulator of spinal plasticity. Here, we shift focus to the periphery and discuss BDNF-TrkB expression on
nociceptors, non-nociceptor sensory neurons, and non-neuronal cells in the periphery as a potential contributor to induction and persistence of pain after SCI. Overall, this
review presents a comprehensive evaluation of large bodies of work that individually focus on pain, DRG, BDNF, and SCI, to understand their interaction in nociceptive processing.