Glutamine synthetase protects the spinal cord against hypoxia-induced and GABAA receptor–activated axonal depressions

Background We investigated the effects of exogenous GS on hypoxia- and GABA A receptor–induced axonal depression in neonatal rats. Methods To assess the effects of GS on spinal cord axons, CAPs were recorded. Hemicords were exposed to hypoxia by 30-minute superfusion with Ringer's solution saturated with 95% N 2 and 5% CO 2 followed by 60-minute exposure to 95% N 2 and 5% CO 2 gassing (N 2 gassing phase) and then 90 minutes of resuperfusion with oxygenated Ringer's solution (resuperfusion phase). Exogenous high GS (15 U) or low GS (1.5 U) was delivered during the N 2 gassing phase. The effects of GS on GABA A receptor–induced axonal depression were analyzed with oxygenated isolated dorsal columns. Results The high GS significantly reduced the decline in the CAP amplitudes during the N 2 gassing and resuperfusion phases ( P = .0185) compared to the hypoxia control. The low GS treatment showed a trend toward recovery during the N 2 gassing and resuperfusion phases, but the effect was not significant ( P = .3953). In isolated dorsal columns, GS significantly reduced the CAP amplitude depression induced by GABA A receptor agonist. Conclusions Our findings suggest that GS had dose-dependent protective effects on the spinal cord against hypoxia-induced axonal depression. It may inhibit the depression of CAP amplitudes by blocking GABA A receptors.