Local Glutamate Level Dictates Adenosine A_2AReceptor Regulation of Neuroinflammation and Traumatic Brain Injury

Selenoprotein S expression in reactive astrocytes following brain injury

“…On the contrary, we have collected evidence indicating that protection by SelS may result from a combination of mechanisms that include SelS ability to cope with ER-stress and inflammation. KA-and trauma-mediated injury induce an intense inflammatory and ER-stress responses that contribute to brain damage (Dai et al, 2010;Motti et al, 2010). In our experiments, SelS suppression and overexpression had a strong impact on astrocytes treated with LPS or ER-stress inducers.…”

Synergistic Roles for G-protein γ3 and γ7 Subtypes in Seizure Susceptibility as Revealed in Double Knock-out Mice

“…Clearly, more studies will be needed to resolve this issue. Providing some insight into these conflicting results, a recent paper suggests that A 2A R activation may switch between neuroprotective and neurodegenerative states depending on existing levels of glutamate (57). Alternatively, D 1 R activation may be responsible for conferring a neuroprotective effect (58).…”

In vitro effect of adenosine A2A receptor antagonist SCH 442416 on the expression of glutamine synthetase and glutamate aspartate transporter in rat retinal M�ller cells at elevated hydrostatic pressure

“…Glutamate excitotoxicity is thought to contribute to a broad variety of neurological diseases including glaucoma (35-39). The previous studies showed that A 2A R inactivation could protect the nerve against various insults including ischemia, excito toxicity, and mitochondrial toxicity (40,41). Our data showed that A 2A receptor antagonist took up the expression of GLAST and GS in Müller cells to accelerate the clearance of extracellular glutamate.…”

“…Holcombe et al reported that IOP threshold of ~70 mmHg for the maintenance of retinal perfusion and IOPs elevated ≤70 mmHg was consistent with the maintenance of GLAST activity in rat glaucomatous model in vivo (30), which was consistent with our result (40 mmHg pressure). Woldemussie et al found that the expression of GLAST increased and remained high for 2 months, following the elevation of IOP (30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40) in rat glaucomatous models in vivo, however, the expression of GS showed little change for the first 3 weeks (13). Nonetheless, Zhang et al reported that the induced expression of GS was observed as early as 24 h following the IOP in elevation in the rat models of acute intraocular hypertension (31).…”