Cahill Catherine M, Dray Andy, Coderre Terence J
Department of Pharmacology and Toxicology, Queen's University, Kingston, ON, Canada.
Neuropharmacology. 2003 Sep;45(4):543-52. doi: 10.1016/s0028-3908(03)00192-8.
It is without dispute that the treatment of neuropathic pain is an area of largely unmet medical need. Available analgesics, such as morphine, either have minimal effects in neuropathic pain patients, or are not always well tolerated due to concurrent adverse effects. The chronicity of neuropathic pain is thought to be related to many neurochemical changes in the dorsal root ganglia (DRG) and spinal cord, including a reduction in the retrograde transport of nerve growth factor (NGF). In this study, we have determined the ability of chronic intrathecal (i.t.) infusion of NGF to reverse neuropathic pain symptoms and to restore morphine's effectiveness in an animal model of neuropathic pain. Seven days after sciatic nerve constriction injury, NGF was administered to the spinal cord by continuous infusion (125 ng/microl/h) via osmotic pumps attached to chronically implanted i.t. catheters. Spinal infusion of NGF did not affect the expression of tactile allodynia or thermal (hot) hyperalgesia in neuropathic rats, although it significantly increased cold water responses frequency at day 14. Following infusion of vehicle, i.t. morphine (20 microg) was ineffective in altering somatosensory thresholds in neuropathic rats. In contrast, morphine substantially attenuated the neuropathy-induced warm and cold hyperalgesia, as well as tactile allodynia, in neuropathic rats chronically infused with i.t. NGF. In addition, we demonstrate that i.t. morphine-induced antinociception was augmented by a cholecystokinin (CCK) antagonist in animals chronically infused with i.t. antibodies directed against NGF. We hypothesize that NGF is critical in maintaining neurochemical homeostasis in the spinal cord of nociceptive neurons, and that supplementation may be beneficial in restoring and/or maintaining opioid analgesia in chronic pain conditions resulting from traumatic nerve injury.
毫无疑问,神经性疼痛的治疗是一个在很大程度上未被满足的医学需求领域。现有的镇痛药,如吗啡,对神经性疼痛患者要么效果甚微,要么由于同时存在的不良反应而耐受性不佳。神经性疼痛的慢性化被认为与背根神经节(DRG)和脊髓中的许多神经化学变化有关,包括神经生长因子(NGF)逆行运输的减少。在本研究中,我们已经确定了在神经性疼痛动物模型中,慢性鞘内(i.t.)注入NGF逆转神经性疼痛症状以及恢复吗啡有效性的能力。坐骨神经压迫损伤7天后,通过连接到长期植入的i.t.导管的渗透泵持续注入(125 ng/微升/小时)NGF至脊髓。脊髓注入NGF对神经性大鼠的触觉异常性疼痛或热(热)痛觉过敏的表达没有影响,尽管它在第14天显著增加了冷水反应频率。注入赋形剂后,i.t.吗啡(20微克)对改变神经性大鼠的体感阈值无效。相比之下,在长期注入i.t. NGF的神经性大鼠中,吗啡显著减轻了神经病变诱导的温热和冷痛觉过敏以及触觉异常性疼痛。此外,我们证明在长期注入针对NGF的i.t.抗体的动物中,胆囊收缩素(CCK)拮抗剂增强了i.t.吗啡诱导的镇痛作用。我们假设NGF在维持伤害性神经元脊髓中的神经化学稳态方面至关重要,并且补充NGF可能有助于在由创伤性神经损伤引起的慢性疼痛状况中恢复和/或维持阿片类镇痛作用。