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P. Bu, J.D. Stittsworth, Jr., T. Dinh, E.B. Stubbs, Jr., J.I. Perlman; The Effect of Short-Duration Pressure-Induced Ischemia on Retinal Function in GLAST Knockout Mice . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2928.
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Purpose: Disturbances in neurotransmitter distribution have been reported in normal mice retina after ischemia. It has been postulated that these changes may be a consequence of glutamate excitotoxicity secondary to defects in the glutamate transport protein GLAST. The purpose of this study was to determine the consequences of glutamate transporter deficiencies on the retinal distribution of neurotransmitters after ischemia. Methods: Five to six month old GLAST knockout mice (n=3) and wild type littermates (n=3) were used for this study. Animals were subjected to elevated intraocular pressure of 110 mmHg in one eye for 5 minutes. The other eye served as a control. Immunolocalization of glutamate (GLU) and glutamine (GLN) was determined by immunohistochemistry with silver intensification. Electroretinograms (ERGs) were recorded before and 24 hours after ischemic insult. Results: The absence of GLAST transporter in the homozygous knockout was confirmed by the absence of GLAST immunoreactivity in the retina as compared to littermate controls. The ERG b- wave of the GLAST-deficient mice was 200±44 µV compared to 244±10µV for wild type control. At 24 hours following a 5 min duration of retinal ischemia the b- wave was reduced to 131±24µV and 161±79µV, for GLAST and control mice, respectively. The overall reduction in amplitude was determined to be equivalent. GLU and GLN immunoreactivity in untreated GLAST-deficient mice was not significantly different from age matched wild type controls either before or 24 hours after 5 minutes of pressure-induced retinal ischemia. Conclusions: For short ischemic durations, there appeared to be no adverse consequences of GLAST glutamate transporter deficiencies on ERG b-wave and neurotransmitter distribution following retinal ischemia. These findings suggest the existence of a compensating mechanism for glutamate transport in GLAST knockout mice. The effect of longer ischemic durations will be elucidated in future studies.
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