CALCIUM-DEPENDENT INACTIVATION OF SYNAPTIC NMDA RECEPTORS IN HIPPOCAMPAL-NEURONS

被引:139
作者
ROSENMUND, C
FELTZ, A
WESTBROOK, GL
机构
[1] OREGON HLTH SCI UNIV,VOLLUM INST,PORTLAND,OR 97201
[2] OREGON HLTH SCI UNIV,DEPT NEUROL,PORTLAND,OR 97201
[3] CNRS,NEUROBIOL CELLULAIRE LAB,F-67084 STRASBOURG,FRANCE
关键词
D O I
10.1152/jn.1995.73.1.427
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
1. We examined whether synaptically activated N-methyl-D-aspartate (NMDA) receptors are regulated by intracellular calcium in cultured hippocampal neurons by comparing excitatory postsynaptic currents (EPSCs) to the previously described calcium-dependent regulation of whole cell NMDA currents. Standard whole cell recording and fast application methods were used. 2. Low-frequency (0.2 Hz) stimulation of EPSCs in the presence of 2-amino-5-phosphonovalerate (AP5) evoked a constant amplitude alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated EPSC. On removal of AP5 in Ca2+-containing solutions, the amplitude of the slow NMDA receptor-mediated EPSC decreased by similar to 50% during the next 10 stimuli. The decrease in the EPSC was dependent on the extracellular calcium concentration and stimulus frequency, consistent with Ca2+-dependent desensitization/inactivation of postsynaptic NMDA receptors. A whole cell prepulse of NMDA (10 mu M, 10 s) in Ca2+-containing solutions inhibited the slow EPSC to a similar degree. A series of slow EPSCs also produced Ca2+-dependent inactivation of whole cell NMDA currents evoked in low calcium solutions. 3. These results demonstrate that synaptic NMDA receptors are inactivated by intracellular calcium and that calcium entry through synaptically activated NMDA receptors is sufficient to provide feedback inhibition of the slow EPSC.
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页码:427 / 430
页数:4
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