Núcleo de Neurociências (NNC), Departamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas, Bloco A4, Sala 168, Universidade Federal de Minas Gerais (UFMG), Avenida Antônio Carlos 6627, 31270-901 Belo Horizonte, Brazil.
Neurosci Lett. 2012 Feb 21;510(1):20-3. doi: 10.1016/j.neulet.2011.12.062. Epub 2012 Jan 8.
Although neuroimmune interactions associated with the development of pain sensitization in models of neuropathic pain have been widely studied, there are some aspects that require further investigation. Thus, we aimed to evaluate whether the local intraneural or perineural injections of dexamethasone, an efficacious anti-inflammatory and immunosuppressant drug, delays the development of both thermal hyperalgesia and mechanical allodynia in an experimental model of neuropathic pain in rats. Hargreaves and electronic von Frey tests were applied. The chronic constriction injury (CCI) of right sciatic nerve was performed. Single intraneural dexamethasone administration at the moment of constriction delayed the development of sensitization for thermal hyperalgesia and mechanical allodynia. However, perineural administration of dexamethasone, at the highest dose, did not delay experimental pain development. These results show that inflammation/immune response at the site of nerve lesion is an essential trigger for the pathological changes that lead to both hyperalgesia and allodynia. In conclusion, this approach opens new opportunities to study cellular and molecular neuroimmune interactions associated with the development of pain derived from peripheral neuropathies.
尽管神经免疫相互作用与神经病理性疼痛模型中疼痛敏化的发展有关，已经得到了广泛的研究，但仍有一些方面需要进一步研究。因此，我们旨在评估地塞米松（一种有效的抗炎和免疫抑制剂药物）的局部神经内或神经周注射是否会延迟大鼠神经病理性疼痛模型中热痛觉过敏和机械性痛觉过敏的发展。应用 Hargreaves 和电子 von Frey 测试。对右侧坐骨神经进行慢性缩窄性损伤（CCI）。在缩窄的同时进行单次神经内给予地塞米松可延迟敏化热痛觉过敏和机械性痛觉过敏的发展。然而，神经周给予地塞米松（最高剂量）并不能延迟实验性疼痛的发展。这些结果表明，神经损伤部位的炎症/免疫反应是导致痛觉过敏和痛觉过敏的病理变化的必要触发因素。总之，这种方法为研究与外周神经病变引起的疼痛发展相关的细胞和分子神经免疫相互作用开辟了新的机会。
