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umerous studies have implicated glutamate-induced neurotoxicity as being related to the pathogenesis of glaucomatous optic neuropathy. Glutamate homeostasis is mainly controlled by the uptake of glutamate and antioxidative process. Unfortunately since we have no idea to measure intercellular or tissue glutamate concentration precisely, the actual mechanism of glutamate-induced cell death still remains unclear. Glutamate transporters become one of the targets to clarify the glutamate homeostasis in glaucoma. Park et al. (1419) investigated time-dependent change of GLAST and GLT-1 expression in ocular hypertension rat model by Western blot and immunohistochemical analysis. Both analysis indicated GLAST expression was stable, but GLT-1 gradually increased during the ocular hypertension. GLAST mainly expressed in Muller cells may be a housekeeping protein independent of ocular hypertension, but GLT-1 may have a protective role in glaucoma. So far, the studies as to glutamate transporter expression have been still controversial. One of the reasons is the difference among the glaucoma models. Cauterization, injection, hypertonic saline, glutamate, or laser have all been used to induce experimental ocular hypertension. Each procedure has pros and cons. Ideal glaucoma models with less tissue damage must be developed in future. GLT-1 has been expressed mainly in cone photoreceptors and some bipolar cells. The contribution of GLT-1 with this specific expression pattern to the inner layers with RGC has not been discussed. Also, the other transports, EAAC1, EAAT4 and 5 must be involved in the glutamate homeostasis. Thus, the real glutamate world in glaucoma may be pretty complicated. Based on this interesting phenomenon, further studies are required.