CAJ | 학술논문

我们实验室以前发现,视网膜视锥与亮度型水平细胞(1uminosity-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.
아문실험실이전발현,시망막시추여량도형수평세포(1uminosity-type horizontal cell,LHC)지간적돌촉전체효솔구유가소성.중복성자격홍민시추증가료LHC대홍광적초겁화반응폭도,이차저충증강작용시가역적.재본문중,아문운용세포내기록기술화약이학분석적방법래고찰중복성홍광자격인기적반응증강적가능궤제.당통과포내주사Ca2+적오합제EGTA래강저LHC내적Ca2+농도후,중복성홍광인기적반응증강피억제,제시돌촉후개신호시반응증강적일개중요인소.령외,반응증강현상환가이피개리자통투적AMPA수체(Ca2+-permeable AMPA receptor,CP-AMPAR)적길항제조단,설명통과개리자통투적곡안산수체내류적Ca2+여포내Ca2+농도적개변유관.진일보발현,포외관류ryanodine혹caffeine야가이소제반응증강현상,설명유개유도적개석방(calcium-induced calcium release,CICR)인기적개신호가능야삼여료반응증강현상적산생.결과제시,CICR화CP-AMPAR여중복성홍광자격인기적LHC대홍광적반응증강유관.
It was previously found that the efficacy of synaptic transmission between retinal cone systems and luminosity-type horizontal cells (LHCs) was activity-dependent. Repetitive activation of red-cone pathway increased the LHC's hyperpolarizing response to red light, and the response enhancement was reversible. In this study, intracellular recording and pharmacological method were applied to investigate the mechanism(s) underlying red-flickering-induced response enhancement. Lowering intracellular Ca2+ in the 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 potent antagonist of Ca2+-permeable AMPA receptor (CP-AMPAR), which suggests the possibility that Ca2+ influx via glutamate-gated calcium channels is related to the changes of [Ca2+]i. Furthermore, the administration of ryanodine or caffeine also attenuated the phenomenon, which gives evidence that the local calcium signal caused by intracellular calcium-induced calcium release (CICR) may be involved. Taken together, our data implicate that postsynaptic CICR and CP-AMPAR are related to the activity-dependent response enhancement.