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Inhibition by intracellular Mg(2+) of recombinant N-methyl-D-aspartate receptors expressed in Chinese hamster ovary cells.
J Pharmacol Exp Ther. 2000 Mar; 292(3):1104-10.JP

Abstract

Intracellular Mg(2+) (Mg(i)(2+)) inhibits the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors in cultured cortical neurons. To examine the effects of Mg(i)(2+) 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 Mg(i)(2+). The voltage dependence of control (0 Mg(i)(2+)) 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 Mg(i)(2+) 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 Mg(i)(2+) has uniform effects on the native NMDA receptors expressed in cortical neurons. Furthermore, inhibition by Mg(i)(2+) 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 Mg(i)(2+) inhibition could not result from poor control of voltage or Mg(i)(2+) 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 Mg(i)(2+).

Authors+Show Affiliations

Li-Smerin Y
Department of Neuroscience, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
Aizenman E
No affiliation info available
Johnson JW
No affiliation info available

MeSH

AnimalsCHO CellsCricetinaeMagnesiumPatch-Clamp TechniquesReceptors, N-Methyl-D-AspartateRecombinant Proteins

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

10688629

Citation

Li-Smerin, Y, et al. "Inhibition By Intracellular Mg(2+) of Recombinant N-methyl-D-aspartate Receptors Expressed in Chinese Hamster Ovary Cells." The Journal of Pharmacology and Experimental Therapeutics, vol. 292, no. 3, 2000, pp. 1104-10.
Li-Smerin Y, Aizenman E, Johnson JW. Inhibition by intracellular Mg(2+) of recombinant N-methyl-D-aspartate receptors expressed in Chinese hamster ovary cells. J Pharmacol Exp Ther. 2000;292(3):1104-10.
Li-Smerin, Y., Aizenman, E., & Johnson, J. W. (2000). Inhibition by intracellular Mg(2+) of recombinant N-methyl-D-aspartate receptors expressed in Chinese hamster ovary cells. The Journal of Pharmacology and Experimental Therapeutics, 292(3), 1104-10.
Li-Smerin Y, Aizenman E, Johnson JW. Inhibition By Intracellular Mg(2+) of Recombinant N-methyl-D-aspartate Receptors Expressed in Chinese Hamster Ovary Cells. J Pharmacol Exp Ther. 2000;292(3):1104-10. PubMed PMID: 10688629.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition by intracellular Mg(2+) of recombinant N-methyl-D-aspartate receptors expressed in Chinese hamster ovary cells. AU - Li-Smerin,Y, AU - Aizenman,E, AU - Johnson,J W, PY - 2000/2/25/pubmed PY - 2000/3/25/medline PY - 2000/2/25/entrez SP - 1104 EP - 10 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 292 IS - 3 N2 - Intracellular Mg(2+) (Mg(i)(2+)) inhibits the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors in cultured cortical neurons. To examine the effects of Mg(i)(2+) 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 Mg(i)(2+). The voltage dependence of control (0 Mg(i)(2+)) 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 Mg(i)(2+) 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 Mg(i)(2+) has uniform effects on the native NMDA receptors expressed in cortical neurons. Furthermore, inhibition by Mg(i)(2+) 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 Mg(i)(2+) inhibition could not result from poor control of voltage or Mg(i)(2+) 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 Mg(i)(2+). SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/10688629/Inhibition_by_intracellular_Mg_2+__of_recombinant_N_methyl_D_aspartate_receptors_expressed_in_Chinese_hamster_ovary_cells_ DB - PRIME DP - Unbound Medicine ER -