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ACTIVATION OF GLUTAMINE SYNTHETASE IS A NEW THERAPEUTIC STRATEGY TO TREAT CHRONIC STRESS-INDUCED DEPRESSIVE DISORDER
Jae Soon Kangand 6 co-authors
College of Medicine, Geyonsang National University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-267
Presentation
Date TBA
Board: PS02-07PM-267
Event Information
Poster Board
PS02-07PM-267
Poster
View posterAbstract
Glutamine synthetase (GS) plays a crucial role in the homeostasis of the glutamate–glutamine cycle in the brain. Hypoactive GS causes depressive behaviors. Under chronic stress, GS has no change in expression, but its activity is decreased due to nitration of tyrosine (Tyr). Thus, we speculate that agents that prevent nitration or facilitate denitration of GS would be candidates for new antidepressants. Using human recombinant GS and mouse lysate from the medial prefrontal cortex, we demonstrated that Tyr (0.0313−0.5 μM) dose-dependently protected GS activity against peroxynitrite-induced Tyr-nitration of GS. Diet supplementation with Tyr exerted significant antidepressant effects in a chronic immobilization stress (CIS) depression mouse model. We further found that dipeptides, such as tyrosyl-glutamine (YQ), which possess suitable chemical properties for medicine, also increased GS activity both in vitro and in vivo, and exerted antidepressant effects. In addition, D-form Tyr (DY), an enantiomer of L-form Tyr, and DYQ also showed antidepressant effects in a dose-dependent manner in CIS-induced depression mice. The activation of GS was achieved by a decrease in Tyr-nitration, in other words, Tyr denitration. Therefore, this study demonstrates that the activation of GS could be a new strategy to treat depression and other GS-related diseases.
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