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Expression of N‐methyl‐D‐aspartate (NMDA) and non‐NMDA glutamate receptor genes in neuroblastoma, medulloblastoma, and other cell lines
Author(s) -
Yoshioka Akira,
Ikegaki Naohiko,
Williams Margaret,
Pleasure David
Publication year - 1996
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19961015)46:2<164::aid-jnr4>3.0.co;2-f
Subject(s) - excitotoxicity , nmda receptor , kainate receptor , biology , ampa receptor , glutamate receptor , microbiology and biotechnology , neuroblastoma , kainic acid , medulloblastoma , receptor , cell culture , cancer research , biochemistry , genetics
We evaluated expression of N‐methyl‐D‐aspartate (NMDA) and non‐NMDA glutamate receptor (GluR) genes by reverse transcriptase‐polymerase chain reaction (RT‐PCR) and Southern blotting in nine established cell lines: rat CG‐4 (oligodendroglial lineage) and RINm5F insulinoma cells; human CHP134, SMS‐KCNR, SKNSH, and Nb69 neuroblastoma cells; and human D384Med, D425Med, and D458Med medulloblastoma cells. CG‐4 expressed mRNAs encoding GluR2–7, KA‐1, and KA‐2 non‐NMDA GluR (Yoshioka et al.: J Neurochem 64:2442–2448, 1995) and NR1 (NMDAR1) and NR2D NMDA GluR. After differentiation to oligodendrocyte‐like cells, CG‐4 also expressed NR2B mRNA. Rat insulinoma cells expressed GluR5, and KA‐2 non‐NMDA and NR1 and NR2D NMDA GluR mRNAs. The four human neuroblastoma lines all expressed mRNAs encoding GluR2–4, 6, 7 and KA‐1 non‐NMDA and NR1 NMDA GluR, and the three human medulloblastoma cell lines all expressed mRNAs encoding GluR1, 6 and KA‐1, but none of the NMDA GluRs. Whereas CG‐4 is susceptible to kainate excitotoxicity, treatment of insulinoma, neuroblastoma, and medulloblastoma lines with L‐glutamate, kainate, α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA), or NMDA failed to cause cell damage or to augment 45 Ca 2+ influx. Thus, despite expressing a variety of non‐NMDA and NMDA GluR genes, the human neuroblastoma and medulloblastoma and rat insulinoma lines failed to assemble Ca 2+ ‐permeable NMDA or non‐NMDA GluR channels. This failure confers protection against excitotoxicity and may contribute to progression of tumors of these types. © 1996 Wiley‐Liss, Inc.