Abstract
Psychiatric diseases and metabolic disorders frequently cooccur, yet the mechanisms underlying this interaction remain unknown. The aim of this study was to determine the role of glucocorticoid receptor (GR) phosphorylation in the comorbidity of metabolic and psychiatric disorders. Neonatal Sprague-Dawley rats were subcutaneously injected with monosodium glutamate (MSG) every 2days for 10days after birth. Metabolic and behavioral tests were performed 12weeks later. Golgi staining and transmission electron microscopy (TEM) were performed to evaluate synaptic structural plasticity. Changes in GR phosphorylation and the BDNF/TrkB pathway were evaluated by western blotting and immunofluorescence. We found that MSG-treated rats displayed significant metabolic abnormalities accompanied by anxiogenic and depressive behaviors, an altered synaptic ultrastructure and the loss of dendritic spines. The expression of phosphorylated GR was reduced in the brain. Furthermore, a specific agonist of BDNF/TrkB significantly reversed the reduction in GR phosphorylation, as well as the metabolic and behavioral outcomes. These findings indicate that a decrease in BDNF/TrkB pathway-dependent GR phosphorylation is a long-term effect of MSG treatment that may contribute to metabolic and behavioral disturbances.
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