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J Neurophysiol 79: 1124-1126, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 79 No. 2 February 1998, pp. 1124-1126
Copyright ©1998 The American Physiological Society

RAPID COMMUNICATION


Zn2+ Blocks the NMDA- and Ca2+-Triggered Postexposure Current Ipe in Hippocampal Pyramidal Cells

Qiang X. Chen, Katherine L. Perkins, and Robert K. S. Wong

Department of Pharmacology, State University of New York Health Science Center, Brooklyn, New York 11203

Chen, Qiang X., Katherine L. Perkins, and Robert K. S. Wong. Zn2+ blocks the NMDA- and Ca2+-triggered postexposure current Ipe in hippocampal pyramidal cells. J. Neurophysiol. 79: 1124-1126, 1998. Whole cell voltage-clamp recordings from acutely isolated hippocampal CA1 pyramidal cells from adult guinea pigs were used to evaluate divalent cations as possible blockers of the postexposure current (Ipe). Ipe is a cation current that is triggered by the rise in intracellular Ca2+ concentration that occurs after the application of a toxic level of N-methyl-D-aspartate (NMDA). Once triggered, Ipe continues to grow until death of the neuron occurs. Ipe may be a critical link between transient NMDA exposure and cell death. Ipe was blocked by micromolar concentrations of Zn2+. The Zn2+ effect had an IC50 of 64 µM and saturated at 500 µM. Prolonged Zn2+ block of Ipe revealed that the maintenance of a steady Ipe is not dependent on Ipe-mediated Ca2+ influx but that the continuous growth in Ipe is dependent on Ipe-mediated Ca2+ influx. The availability of an effective blocker of Ipe should facilitate the investigation of the intracellular activation pathway of Ipe and the role of Ipe in neuronal death.




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