Jurna I
Arzneimittelforschung. 1984;34(9A):1084-8.
The spinal nociceptive system is the target of various pain depressing agents. It is capable to function without control from the brain. It is activated by tissue damage which, by excitation of nociceptive afferents, evokes activity in axons ascending to the brain (sensory nociceptive response) and in spinal reflex pathways (motor and autonomic responses). The prototype of an analgesic agent, morphine, suppresses nociceptive responses by binding to opiate receptors; it imitates the effect of the transmitter(s) released from endorphinergic neurones. Pentobarbital and diazepam reduce nociceptive (and non-nociceptive) responses by acting on the GABA receptor complex; both drugs facilitate the effect of the transmitter GABA which mediates presynaptic inhibition in the spinal cord. Pentobarbital may produce its effects by an additional action on postsynaptic neurone membranes. Clonidine depresses nociceptive responses, probably by imitating the action of the inhibitory transmitter, noradrenaline. Substance P acts as a "synaptic modulator"; it may facilitate or inhibit nociceptive responses. Ceruletide and cholecystokinin octapeptide depress nociceptive motor responses but do not affect the nociceptive sensory response. This indicates that motor and sensory responses of the spinal nociceptive system are not rigidly linked together. With the help of appropriate drugs, it is possible to manipulate them separately.
脊髓伤害性感受系统是各种止痛剂的作用靶点。它能够在不受大脑控制的情况下发挥功能。它由组织损伤激活，通过伤害性传入纤维的兴奋，引发向大脑上行的轴突活动（感觉伤害性反应）以及脊髓反射通路中的活动（运动和自主反应）。镇痛剂的原型吗啡，通过与阿片受体结合来抑制伤害性反应；它模拟了内啡肽能神经元释放的递质的作用。戊巴比妥和地西泮通过作用于GABA受体复合物来降低伤害性（和非伤害性）反应；这两种药物都增强了递质GABA的作用，GABA介导脊髓中的突触前抑制。戊巴比妥可能通过对突触后神经元膜的额外作用来产生其效果。可乐定抑制伤害性反应，可能是通过模拟抑制性递质去甲肾上腺素的作用。P物质作为一种“突触调节剂”；它可能促进或抑制伤害性反应。蛙皮素和胆囊收缩素八肽抑制伤害性运动反应，但不影响伤害性感觉反应。这表明脊髓伤害性感受系统的运动和感觉反应并非紧密相连。借助适当的药物，可以分别对它们进行调控。
