The A2A receptor (A2AR) antagonist has been considered as an attractive option to improve the treatment of
neurological disorders, and the function of A2AR antagonist may inhibit the release of
glutamate and prevent neuron damage. The aim of the present study was to investigate whether
SCH442416 can modulate the
glutamate uptake in
retinal Müller cells under increased hydrostatic pressure. The levels of
glutamine synthetase (GS) and
glutamate aspartate transporter (GLAST) were assessed in
retinal Müller cells under 40 mmHg pressure for 24 h using reverse transcription‑quantitative polymerase chain reaction and western blotting, and a
glutamate uptake assay was performed using a scintillation counting method. Following treatment of the Müller cells with 100 nM
SCH442416 under 40 mmHg pressure for 24 h, the
mRNA and
protein expression levels of GS and GLAST, and
glutamate uptake activity were investigated. Under 40 mmHg pressure, the expression levels of GS and GLAST in the Müller cells, and
glutamate uptake activity were significantly reduced. Treatment with
SCH442416 significantly ameliorated the decreased expression levels of GS and GLAST, and improved the
glutamate uptake activity in the
retinal Müller cells exposed to 40 mmHg pressure, resulting in increased expression levels of GS and GLAST, and increased
glutamate uptake activity in the Müller cells under pressure. These results suggested that
SCH442416 may be a potential candidate as a beneficial
neuroprotective agent for the treatment of
glaucoma by accelerating the clearance of extracellular
glutamate.