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催产素在成年大鼠脊髓后角胶状质细胞层处的镇痛机制 被引量:4

THE MECHANISMS OF OXYTOCIN-INDUCED ANTINOCICEPTION IN SUBSTANTIA GELATINOSA NEURONS OF RAT SPINAL DORSAL HORN
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摘要 目的:探讨催产素在脊髓后角胶状质细胞层的镇痛机制。方法:本研究使用成年雄性SD大鼠,运用椎板切除术取出脊髓腰骶膨大节段(L1~S3),并置于1~3℃的Krebs液中。用切片机制作脊髓横切片,该切片被置于记录槽中并给予Krebs液灌流。运用盲法全细胞膜片钳技术记录催产素对脊髓横切片中胶状质神经元电生理活动的影响。结果:在钳制电压为-70 m V时,灌流催产素(0.5μM/L)3分钟可诱发内向电流;并且该内向电流不能被TTX阻断。但催产素对自发性兴奋性突触后电流无影响。另外催产素增加了γ-氨基丁酸与甘氨酸介导的自发性抑制性突触后电流的频率和振幅,而该增加可被TTX抑制。催产素受体激动剂TGOT能够模拟催产素的效果,诱发胶状质细胞出现内向电流;催产素受体抑制剂d VOT能抑制催产素所引起的内向电流。结论:在脊髓后角胶状质细胞层,催产素通过激活催产素受体引起胶状质细胞的膜去极化,从而引起抑制性神经递质的释放增加,达到抑制疼痛信息传导的效果。 Objective: To examine the mechanisms for oxytocin-induced antinociception in substantia gelatinosa(SG) neurons in the spinal dorsal horn of rats. Methods: Adult male Sprague-Dawley rats were used in this study. A laminectomy was performed to extract a lumbosacral spinal cord enlargement(L1~S3). The spinal cord was immersed in ice-cold(1~3 ℃) Krebs solution. A transverse slice was cut by using a microslicer. The slice was placed in the recording chamber and then perfused with Krebs solution. The blind whole-cell patch-clamp technique was applied to the SG neurons in the spinal cord slices. Results: Superfusion of oxytocin(0.5 μM/L) for 3 minutes induced an inward current at-70 m V which was resistant to TTX. The spontaneous excitatory postsynaptic current was unaffected by oxytocin. However, GABAergic and glycinergic spontaneous inhibitory postsynaptic currents were increased in frequency and amplitude by oxytocin in a manner sensitive to TTX. The oxytocin-induced inward current was mimicked by an oxytocin-receptor agonist TGOT and was inhibited by an oxytocin-receptor antagonist d VOT. Conclusion: The data suggest that oxytocin produces a membrane depolarization in SG neurons, which increases the release of inhibitory transmitters through oxytocin receptor activation.
出处 《中国疼痛医学杂志》 CAS CSCD 2016年第7期501-505,共5页 Chinese Journal of Pain Medicine
基金 广东省自然科学基金(2016A30310035)
关键词 催产素 脊髓后角 膜片钳 突触传导 Oxytocin Spinal dorsal horn Patch-clamp Synaptic transmission
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参考文献19

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