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

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• 作者：Bartłomiej Pochwat ; ^{pochwat@if-pan.krakow.pl" class="auth_mail" title="E-mail the corresponding author} ; Gabriel Nowak ; Bernadeta Szewczyk
• 关键词：Magnesium ; GAD-67 ; Olfactory bulbectomy ; Chronic mild stress ; NMDA
• 刊名：Pharmacological Reports
• 出版年：2016
• 出版时间：October 2016
• 年：2016
• 卷：68
• 期：5
• 页码：881-885
• 全文大小：742 K

文摘

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.