Mechanism of descending pain control system in the spinal cord

用全细胞膜片钳技术记录脊髓胶状质（SG）神经元，探讨下行痛控制系统的机制，在大多数SG神经元中，5-羟色胺（5-HT）、去甲肾上腺素（NA）和乙酰胆碱（ACh）通过增加钾电导诱发外向电流。NA、5-HT和ACh可增加IPSC的自发频率。NA和ACh的作用分别由α 1和毒蕈碱受体介导。参与5-HT作用的受体亚型尚不清楚。TTX可部分阻断上述效应，尤其是消除大幅度的IPSC，提示这些IPSC中有一部分是由体-树突棘作用引起的; NA、5-HT和ACh可增加TTX存在时的小型IPSC频率，提示NA、5-HT和ACh通过突触前机制增加抑制性递质释放。NA和ACh的作用分别由α 1和毒蕈碱受体介导。这些结果表明，下行痛控制系统抑制SG神经元至少有两种机制：1）通过激活钾传导引起超极化; 2）通过突触前和突触后机制激活GABA和甘氨酸抑制性中间神经元。

Whole cell patch clamp recordings were made from substantia gelatinosa (SG) neurons to investigate the mechanisms of descending pain control systems in spinal cord level.In the majority of SG neurons, serotonine (5-HT), noradrenaline (NA) and acetylcholine (ACh) evoked outward currents by increasing potassium conductance. These effects were mediated by 5-HTIA alpha2 and muscarinic receptors, respectively.NA,5-HT and ACh increased the frequency of spontaneous IPSCs. The effects of NA and ACh were mediated by alpha1 and muscarimic receptors, respectively. The receptor subtype involed in 5-HT action was not clear. These effects were partially blocked by TTX,especially large amplitude of IPSCs were eliminated by TTX,suggesting that a portion of these IPSCs were results from soma-dendritic spiking.NA,5-HT and ACh increased the frequency of miniature-IPSCs in the presence of TTX,suggesting thar NA,5-HT and ACh increase inhibitory transmitter release through presynaptic mechanism. The effects of NA and ACh were mediated by alpha1 and muscarinic receptors, respectively. The receptor subtype involved in 5-HT action was not clear.These results indicate that there are at least two mechanisms by which the descending pain control systems inhibit SG neuros : 1) hyperpolarization through activation of K conductance ; 2) activation of GABA and glycine-containing inhibitory interneurons through pre-and postsynaptic mechanisms.