Basbaum A I, Fields H L
Ann Neurol. 1978 Nov;4(5):451-62. doi: 10.1002/ana.410040511.
The anatomy, physiology, and pharmacology of an intrinsic neural network that monitors and modulates the activity of pain-transmitting neurons is reviewed. This system can be activated by opiate administration or by electrical stimulation of discrete brainstem sites. Evidence is presented that its pain-suppressing action is mediated in part by endogenous opiatelike compounds (endorphins). This pain suppression system is organized at three levels of the neuraxis: midbrain, medulla, and spinal cord. Activation of neurons in the midbrain periaqueductal gray matter (by electrical stimulation, opiates, and possibly psychological factors) excites neurons of the rostral medulla, some of which contain serotonin. The medullary neurons, in turn, project to and specifically inhibit the firing of trigeminal and spinal pain-transmission neurons. As part of a negative feedback loop, the output of the pain transmission neurons, i.e., pain itself, is an important factor in activating the pain-suppression system. A neural model which incorporates the experimental findings is proposed, and the clinical implications of the model are discussed.
本文综述了一个监测和调节痛觉传递神经元活动的内在神经网络的解剖学、生理学和药理学。该系统可通过给予阿片类药物或电刺激离散的脑干部位来激活。有证据表明，其止痛作用部分是由内源性阿片样化合物（内啡肽）介导的。这个疼痛抑制系统在神经轴的三个水平上组织起来：中脑、延髓和脊髓。中脑导水管周围灰质中的神经元被激活（通过电刺激、阿片类药物以及可能的心理因素）会兴奋延髓头端的神经元，其中一些含有5-羟色胺。延髓神经元进而投射到三叉神经和脊髓痛觉传递神经元并特异性抑制其放电。作为负反馈回路的一部分，痛觉传递神经元的输出，即疼痛本身，是激活疼痛抑制系统的一个重要因素。本文提出了一个包含实验结果的神经模型，并讨论了该模型的临床意义。
