首页|期刊导航|中华医学杂志（英文版）|D-AP5 blocks the increase of intracellular free Ca2+ induced by glutamate
in isolated cochlear IHCs
中华医学杂志（英文版）2002，Vol.115Issue(1)：89-93,5.
D-AP5 blocks the increase of intracellular free Ca2+ induced by glutamate in isolated cochlear IHCs
D-AP5 blocks the increase of intracellular free Ca2+ induced by glutamate in isolated cochlear IHCs
摘要
Abstract
Objective To investigate the effect of D-AP5 (D-2-amino-5-phosphonopentanoate, a specific NMDA-antagonist) on the increase of intracellular free Ca2+ concentration (［Ca2+］i) induced by glutamate in isolated cochlear inner hair cells (IHCs), and to detect the autoreceptors of the IHC membrane. Methods When a laser scanning confocal microscope (LSCM) was used, the exogenous glutamate (Glu)-induced changes in ［Ca2+］i of isolated IHCs and OHCs of guinea pig cochlea were observed with fluo-3, a fluorescent probe for ［Ca2+］i. After D-AP5 or CNQX (6--cyano--7--nitroguinoxaline--2, 3--dione, a specific AMPA- antagonist) was administrated, the exogenous glutamate (Glu)-induced changes in ［Ca2+］i of isolated IHCs were recorded. Results In the presence of a low concentration Glu (3.85?μmol/L), there was an increase of ［Ca2+］i in IHCs, whereas there was no change in OHCs. When 50?μmol/L of D-AP5 was administrated in advance, Glu did not induce a corresponding increase in ［Ca2+］i in IHCs, and 50?μmol/L of CNQX did not completely block the increase of ［Ca2+］i in IHCs. Conclusions These results suggest that the autoreceptors existing in the IHC membrane are mainly of NMDA type, while there are relatively few AMPA receptors. Exogenous Glu is capable of increasing ［Ca2+］i in IHCs by acting on the NMDA autoreceptor of IHCs in a positive feedback manner.关键词
glutamate/cochlear inner hair cell/intracellular free Ca2+/autoreceptorKey words
glutamate/cochlear inner hair cell/intracellular free Ca2+/autoreceptor分类
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李兴启,孙建和,于宁,孙燕荣,谭祖林,姜泗长,李楠,周春喜..D-AP5 blocks the increase of intracellular free Ca2+ induced by glutamate in isolated cochlear IHCs[J].中华医学杂志（英文版）,2002,115(1):89-93,5.基金项目
This project was supported by grants from the National Natural Science Foundation of China (No. 39870797) （No. 39870797）
