Altier N, Stewart J
Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montreal, Quebec, Canada.
Life Sci. 1999;65(22):2269-87. doi: 10.1016/s0024-3205(99)00298-2.
Opioid and psychostimulant drugs have long been used for the relief of chronic pain in the clinical situation. Animal studies confirm that these drugs alleviate persistent or tonic pain. Little is known, however, about the neural systems underlying the suppression of tonic pain except that they are different from those mediating the suppression of phasic (i.e., sharp and short-lasting) pain. Although spinal and brainstem-descending pain suppression mechanisms play a role in mediating the inhibition of tonic pain, it appears that this response is additionally mediated by the activation of mechanisms lying rostral to the brainstem. Recent studies suggest that the activation of mesolimbic dopamine (DA) neurons, arising from the cell bodies of the ventral tegmental area (VTA) and projecting to the nucleus accumbens (NAcc), plays an important role in mediating the suppression of tonic pain. Other studies suggest that this pain-suppression system involving the activation of mesolimbic DA neurons is naturally triggered by exposure to stress, through the endogenous release of opioids and substance P (SP) in the midbrain.
阿片类药物和精神刺激药物长期以来一直用于临床缓解慢性疼痛。动物研究证实,这些药物可减轻持续性或紧张性疼痛。然而,除了它们与介导抑制相性(即尖锐且持续时间短)疼痛的神经系统不同之外,对于抑制紧张性疼痛的神经系统知之甚少。尽管脊髓和脑干下行性疼痛抑制机制在介导紧张性疼痛的抑制中发挥作用,但这种反应似乎还由脑干前方机制的激活介导。最近的研究表明,源自腹侧被盖区(VTA)细胞体并投射到伏隔核(NAcc)的中脑边缘多巴胺(DA)神经元的激活在介导紧张性疼痛的抑制中起重要作用。其他研究表明,这种涉及中脑边缘DA神经元激活的疼痛抑制系统是通过中脑内阿片类药物和P物质(SP)的内源性释放,由暴露于应激自然触发的。