Kyung Park Yun, Jun Jung Sung, Kwak Jiyeon, Kim Jun
Department of Physiology and Biophysics, Seoul National University College of Medicine, 28 Yongon-dong, Chongno-gu, Seoul, Republic of Korea.
Biochem Biophys Res Commun. 2002 Jul 26;295(4):929-36. doi: 10.1016/s0006-291x(02)00790-8.
We have investigated the effect of hypoxia on the excitatory synaptic transmission in the substantia gelatinosa neurons using perforated-patch-clamp configuration. Brief periods of hypoxia induced a depression in the evoked excitatory postsynaptic current (eEPSC) amplitude. The hypoxia-induced depression of eEPSC was not observed in the presence of theophylline, a nonselective adenosine receptor antagonist, and DPCPX, a selective adenosine receptor A1 antagonist. Application of adenosine (100 microM) also depressed eEPSC in a similar way as with hypoxia. This adenosine-induced depression of eEPSC was inhibited by DPCPX. Hypoxia and exogenous adenosine decreased the frequency of the spontaneous excitatory postsynaptic current (sEPSC) but not the amplitude of sEPSC and increased the paired-pulse ratio. From these results, it is suggested that acute hypoxia depresses the excitatory synaptic transmission by activating the presynaptic adenosine A1 receptor.
我们使用穿孔膜片钳技术研究了缺氧对脊髓背角胶状质神经元兴奋性突触传递的影响。短暂缺氧可导致诱发兴奋性突触后电流(eEPSC)幅度降低。在存在非选择性腺苷受体拮抗剂茶碱和选择性腺苷A1受体拮抗剂DPCPX的情况下,未观察到缺氧诱导的eEPSC降低。应用腺苷(100 microM)也以与缺氧类似的方式降低eEPSC。DPCPX可抑制这种腺苷诱导的eEPSC降低。缺氧和外源性腺苷降低了自发性兴奋性突触后电流(sEPSC)的频率,但不影响sEPSC的幅度,并增加了配对脉冲比率。从这些结果表明,急性缺氧通过激活突触前腺苷A1受体抑制兴奋性突触传递。