Kindling increases N-methyl-d-aspartate potency at single N-methyl-d-aspartate 
channels in dentate gyrus granule cells

Köhr, Georg; Mody, Istvan

doi:10.1016/0306-4522(94)90336-0

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Kindling increases N-methyl-d-aspartate potency at single N-methyl-d-aspartate channels in dentate gyrus granule cells

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Köhr, Georg
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;
Directly responsible to the Managing Director, Max Planck Institute for Medical Research, Max Planck Society;
Georg Köhr Group, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Köhr, G., & Mody, I. (1994). Kindling increases N-methyl-d-aspartate potency at single N-methyl-d-aspartate channels in dentate gyrus granule cells. Neuroscience, 62(4), 975-981. doi:10.1016/0306-4522(94)90336-0.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0019-A8C2-7

Abstract

Dose-response studies of N-methyl-D-aspartate channel openings were carried out using cell-attached patches in dentate gyrus granule cells acutely isolated from control and kindled rats. The tips of the patch electrodes were first filled with regular extracellular solution, followed by backfilling through the shank with the agonist containing solution. As the two solutions joined, the agonist (N-methyl-D-aspartate, 25 microM) steadily diffused to the cell membrane, and the concentration gradually built up resulting in the progressive increase in the opening probability of N-methyl-D-aspartate channels. The reliability of this cell-attached diffusional drug delivery method was tested by determining the concentration dependence of competitive antagonism of N-methyl-D-aspartate induced channel activity by D(-)-2-amino-5-phosphonopentanoic acid. The Ki for D(-)-2-amino-5-phosphonopentanoic acid in the presence of 25 microM N-methyl-D-aspartate was found to be 6.8 microM. Twenty-four hours following the last seizure, N-methyl-D-aspartate channels on kindled neurons were consistently activated by lower N-methyl-D-aspartate concentrations than channels on control granule cells, indicating a higher potency of agonist at epileptic N-methyl-D-aspartate channels. The higher potency of the agonist is most likely a reflection of the long-term alterations in the modulation of N-methyl-D-aspartate receptor function in epileptic neurons.