Abstract
Treatment of the human teratocarcinoma line NTera2/c1.D1 (NT2) with retinoic acid induces terminal neuronal differentiation. In a previous study, we found that the neurons obtained in this way express functional N-methyl- D-aspartate (NMDA) and non-NMDA glutamate receptor channels. We now show by reverse transcriptase-polymerase chain reaction and Southern blotting that these neurons transcribe each of the nine known non-NMDA glutamate receptor genes (GluR1-7, Ka-1, and Ka-2) and that four of these genes (GluR2, GluR6, GluR7, and Ka-1) are also transcribed by undifferentiated NT2 cells. Patch clamp studies demonstrate that individual non-NMDA glutamate receptor channels are readily isolated from NT2-derived neurons and that these channels are potently modulated by the desensitization blocker cyclothiazide. NT2-derived neurons are susceptible to kainate excitotoxicity but are not injured by prolonged exposure to α-amino-3-hydroxy-5-methyl-4- isoxazolepropionate. We expect that the NT2-derived human neuronal culture system will facilitate studies of human neuronal non-NMDA glutamate receptor channels and of the pathophysiology of neuronal excitotoxicity.
Original language | English (US) |
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Pages (from-to) | 482-489 |
Number of pages | 8 |
Journal | Journal of Neurochemistry |
Volume | 63 |
Issue number | 2 |
State | Published - Aug 1994 |
Externally published | Yes |
Keywords
- α-Amino-3- hydroxy-5-methyl-4-isoxazolepropionate
- Cell culture
- Excitotoxicity
- Glutamate receptor channels
- Kainate
- Neurons
- Patch clamp
- Reverse transcriptase- polymerase chain reaction
ASJC Scopus subject areas
- Biochemistry
- Cellular and Molecular Neuroscience