%0 Journal Article %A Yingying Li-Smerin %A Elias Aizenman %A Jon W. Johnson %T Inhibition by Intracellular Mg2+ of RecombinantN-Methyl-d-aspartate Receptors Expressed in Chinese Hamster Ovary Cells %D 2000 %J Journal of Pharmacology and Experimental Therapeutics %P 1104-1110 %V 292 %N 3 %X Intracellular Mg2+ (Mgi2+) inhibits theN-methyl-d-aspartate (NMDA) subtype of glutamate receptors in cultured cortical neurons. To examine the effects of Mgi2+ on recombinant NMDA receptors composed of subunit combinations found in cortical neurons, we expressed heteromeric receptors composed of NR1/NR2A and of NR1/NR2B subunits in Chinese hamster ovary (CHO) cells. We recorded whole-cell currents from the recombinant receptors in the absence and presence of Mgi2+. The voltage dependence of control (0 Mgi2+) NMDA-activated currents obtained from CHO cells transfected with NR1/NR2A and with NR1/NR2B receptors showed outward rectification, a property that has been observed previously in native cortical NMDA receptors. The magnitude and voltage dependence of inhibition by Mgi2+ of NMDA-activated currents were similar in CHO cells transfected with NR1/NR2A receptors, CHO cells transfected with NR1/NR2B receptors, and in cultured neurons expressing native NMDA receptors. These observations suggest that Mgi2+ has uniform effects on the native NMDA receptors expressed in cortical neurons. Furthermore, inhibition by Mgi2+ must not depend on intracellular factors or post-translational receptor modifications that are specific to neurons. Finally, the results indicate that the previously observed differences between whole-cell and outside-out patch measurements of Mgi2+ inhibition could not result from poor control of voltage or Mgi2+ concentration in the dendrites of neurons. The most likely alternative explanation is that patch excision causes an alteration in NMDA receptors that results in more effective inhibition by Mgi2+. The American Society for Pharmacology and Experimental Therapeutics %U https://jpet.aspetjournals.org/content/jpet/292/3/1104.full.pdf