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4 Functional glutamate uptake systems are critical for  maintenance of normal synaptic transmission. Several studies have shown  that in severely ischemic brain regions, massive efflux of excitatory  amino acids (EAAs) results, in large portion, from the reversal of  Na+ -dependent glutamate transporters. This study was  designed to examine the function of the predominant glial transporter,  GLT-1, in a brain area representative of ischemic penumbra.  Spontaneously hypertensive rats were subjected to a 45 min transient  focal ischemia by intraluminal occlusion of the middle cerebral artery  (MCAO). In this model, the core ischemic region resides in the medial  striatum while the surrounding parietal cortex represents a penumbral  area. Temporal profiles of extracellular levels of glutamate  [Glu]e and aspartate [Asp]e were assessed  using microdialysis in the parietal cortex. Preischemic  [Glu]e and [Asp]e were constant and no  changes were observed in sham operated animals. MCAO induced rapid  efflux of EAAs with the peak of 7 and 9 fold increases in  [Glu]e and [Asp]e at 20 min post MCAO,  respectively. Levels of both EAAs returned to baseline prior to  reperfusion. In contrast, a local infusion (reverse microdialysis) of  the GLT-1 selective nontransportable inhibitor, dihydrokainate (DHK, 1  mM) during the ischemic insult,prolonged and increased the efflux of  both EAAs throughout MCAO interval resulting in peak 9 and 16 fold  increases (p&gt;0.05) in [Glu]e and [Asp]e ,  respectively, at 40 min post MCAO. The total ischemic efflux of Glu and  Asp (areas under the curve, AUC) was increased by 70% and 98%.  Infusion of the voltage dependent Na+ channel blocker  tetrodotoxin (TTX, 10 μM) during the ischemic period attenuated the  initial MCAO-induced Glu and Asp efflux from 7 to 2 fold and from 9 to  2 fold, respectively. These data provide the first evidence that within  the ischemic brain penumbra, GLT-1 remains functional and displays no  evidence of reverse transport. In addition, the attenuation of  MCAO-induced EAA efflux by TTX indicates that the source of penumbral  release is primarily neuronal.

GLIAL GLUTAMATE TRANSPORTER GLT-1 DOES NOT REVERSE ITS FUNCTION IN ISCHEMIC PENUMBRA.