LETTER TO THE EDITOR

TL;DRAbstract

Dear Editor, We read with interest the article “Tetramethylpyrazine inhibits activities of glioma cells and glutamate neuroexcitotoxicity: Potential therapeutic application for treatment of gliomas” by Fu et al. (Neuro-Oncology 2008;10:139–152).1 We were surprised that the authors did not examine or discuss the possible role of the N-methyl-D-aspartate (NMDA) type of ionotropic glutamate receptor in mediating glutamate-induced [Ca2+] increase in glioma cells and glioma cell-induced neuro-toxicity. In fact, the NMDA receptor was not mentioned anywhere in the article, although it has been implicated in mediating both glutamate excitotoxicity and glioma growth. There are a number of reasons why the involvement of NMDA receptors should have been investigated, or at least discussed. The study by Fu et al. indicated that tetramethylpyrazine inhibited glioma growth and protected neurons against glioma-induced excitotoxicity. The involvement of non-NMDA glutamate receptors in some glutam

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