EXPRESSION OF N-METHYL-D-ASPARTATE (NMDA) AND NON-NMDA GLUTAMATE-RECEPTOR GENES IN NEUROBLASTOMA, MEDULLOBLASTOMA, AND OTHER CELL-LINES

We evaluated expression of N-methyl-D-aspartate (NMDA) and non-NMDA gl utamate receptor (GluR) genes by reverse transcriptase-polymerase chai n reaction (RT-PCR) and Southern blotting in nine established cell lin es: rat CG-4 (oligodendroglial lineage) and RINm5F insulinoma cells; h uman CHP134, SMS-KCNR, SKNSH, and Nb69 neuroblastoma cells; and human D384Med, D425Med, and D458Med medulloblastoma cells, CG-4 expressed mR NAs 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, Af ter 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 mRN As encoding GluR1, 6 and KA-1, but none of the NMDA GluRs, Whereas CG- 4 is susceptible to kainate excitotoxicity, treatment of insulinoma, n euroblastoma, and medulloblastoma lines with L-glutamate, kainate, pha -amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA), or NMDA failed to cause cell damage or to augment Ca-45(2+) influx, Thus, despite ex pressing a variety of non-NMDA and NMDA GluR genes, the human neurobla stoma and medulloblastoma and rat insulinoma lines failed to assemble Ca2+-permeable NMDA or non-NMDA GluR channels, This failure confers pr otection against excitotoxicity and may contribute to progression of t umors of these types, (C) 1996 Wiley-Liss, Inc.