过刊浏览

我们实验室以前发现，视网膜视锥与亮度型水平细胞(luminosity-type horizontal cell, LHC)之间的突触传递效率具有可塑性。重复性刺激红敏视锥增加了LHC 对红光的超极化反应幅度，而且这种增强作用是可逆的。在本文中，我们运用细胞内记录技术和药理学分析的方法来考察重复性红光刺激引起的反应增强的可能机制。当通过胞内注射Ca2+ 的螯合剂EGTA来降低LHC 内的Ca2+ 浓度后，重复性红光引起的反应增强被抑制，提示突触后钙信号是反应增强的一个重要因素。另外，反应增强现象还可以被钙离子通透的AMPA 受体(Ca2+-permeable AMPA receptor, CP-AMPAR)的拮抗剂阻断，说明通过钙离子通透的谷氨酸受体内流的Ca2+ 与胞内Ca2+ 浓度的改变有关。进一步发现，胞外灌流ryanodine 或caffeine 也可以消除反应增强现象，说明由钙诱导的钙释放(calcium-induced calcium release, CICR)引起的钙信号可能也参与了反应增强现象的产生。结果提示，CICR 和CP-AMPAR 与重复性红光刺激引起的LHC 对红光的反应增强有关。

It was previously found that the efficacy of synaptic transmission between retinal cone systems and luminosity-typehorizontal cells (LHCs) was activity-dependent. Repetitive activation of red-cone pathway increased the LHC’s hyperpolarizingresponse to red light, and the response enhancement was reversible. In this study, intracellular recording and pharmacological methodwere applied to investigate the mechanism(s) underlying red-flickering-induced response enhancement. Lowering intracellular Ca2+ inthe LHC by intracellular injection of Ca2+ chelator EGTA prevented the development of red-flickering-induced response enhancement,which implicates the importance of postsynaptic calcium signal. The response enhancement could also be eliminated by a potentantagonist of Ca2+-permeable AMPA receptor (CP-AMPAR), which suggests the possibility that Ca2+ influx via glutamate-gatedcalcium channels is related to the changes of [Ca2+]i. Furthermore, the administration of ryanodine or caffeine also attenuated thephenomenon, which gives evidence that the local calcium signal caused by intracellular calcium-induced calcium release (CICR) may beinvolved. Taken together, our data implicate that postsynaptic CICR and CP-AMPAR are related to the activity-dependent responseenhancement.