Brain glutamic acid decarboxylase-67 kDa alterations induced by magnesium treatment in olfactory bulbectomy and chronic mild stress models in rats

Background the preclinical results indicate that magnesium,an n-methyl-d-aspartate receptor (nmdar) blocker has anxiolytic and antidepressant-like activity. one of the mechanisms involved in these activities is modulation of glutamate,γ-aminobutyric acid (gaba) system. based on this,the aim of the present study was to investigate the effect of magnesium on the level of glutamic acid decarboxylase-67 kda (gad-67) in the different brain areas in the chronic mild stress (cms) and olfactory bulbectomy (ob) models of depression in rats. methods magnesium (15 mg/kg) was administered intraperitonealy once daily for 14 days in the ob model and for 35 days in the cms model. 24 h after the last dose,the prefrontal cortex (pfc),hippocampus and amygdala were collected and the gad-67 protein level was determined by the western blotting method. results in the ob model,chronic magnesium treatment normalized decreased by ob protein level of gad-67 in pfc. cms did not influence the gad-67 protein level,however magnesium increased gad-67 protein expression in amygdala and pfc of stress rats when compared to vehicle-treated stress group. ob or cms models as well as magnesium treatment did not affect gad-67 protein level in the hippocampus. conclusions obtained results indicate that the antidepressant-like activity of magnesium in cms and ob models of depression is associated with an enhanced expression of gad-67 in the pfc and amygdala. © 2016 institute of pharmacology,polish academy of sciences. published by elsevier sp. z o.o. all rights reserved.