Kerchner Geoffrey A, Zhuo Min
Washington University Pain Center and Departments of Anesthesiology, Anatomy and Neurobiology, and Psychiatry, Washington University School of Medicine, St. Louis, Missouri, 63110, USA.
J Neurophysiol. 2002 Jul;88(1):520-2. doi: 10.1152/jn.2002.88.1.520.
Opioids modify sensory experience at many levels in the CNS. The mechanisms of this action, including the ways opioid receptors affect synaptic transmission, are not yet fully understood. Here we show that the selective activation of mu-opioid receptors suppressed inhibitory transmission between spinal cord dorsal horn neurons in vitro. mu-Opioid receptor activation reduced evoked inhibitory postsynaptic current (eIPSC) amplitude by acting presynaptically, because it altered the paired-pulse ratio, did not affect GABA-evoked currents, and decreased miniature IPSC (mIPSC) frequency. The mechanism of this effect was independent both of presynaptic Ca(2+) entry and of the pathway linking presynaptic kainate (KA) receptors to suppression of inhibitory transmission in the same cells. These data identify mu-opioid receptors as important presynaptic modulators of dorsal horn inhibitory transmission.
阿片类药物在中枢神经系统的多个层面改变感觉体验。这种作用的机制，包括阿片受体影响突触传递的方式，尚未完全阐明。在此我们表明，μ-阿片受体的选择性激活在体外抑制脊髓背角神经元之间的抑制性传递。μ-阿片受体激活通过突触前作用降低诱发的抑制性突触后电流（eIPSC）幅度，因为它改变了配对脉冲比率，不影响GABA诱发的电流，并降低微小IPSC（mIPSC）频率。这种效应的机制既独立于突触前Ca(2+)内流，也独立于将突触前海人藻酸（KA）受体与同一细胞中抑制性传递抑制相联系的途径。这些数据确定μ-阿片受体是背角抑制性传递重要的突触前调节剂。
