Antidepressant- and anxiolytic-like activity of magnesium in mice
The antidepressant- and anxiolytic-like effects of magnesium, an N-methyl- d-aspartate (NMDA) glutamate receptor inhibitor, were studied in mice using the forced swim test and elevated plus-maze test, respectively. The doses of 20 and 30 mg Mg/kg, reduced immobility time in the forced swim test exer...
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Published in | Pharmacology, biochemistry and behavior Vol. 78; no. 1; pp. 7 - 12 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Elsevier Inc
01.05.2004
Elsevier Science |
Subjects | |
Online Access | Get full text |
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Summary: | The antidepressant- and anxiolytic-like effects of magnesium, an
N-methyl-
d-aspartate (NMDA) glutamate receptor inhibitor, were studied in mice using the forced swim test and elevated plus-maze test, respectively. The doses of 20 and 30 mg Mg/kg, reduced immobility time in the forced swim test exerting antidepressant-like activity. In the elevated plus-maze test, magnesium at the same doses produced anxiolytic-like effect. The doses of magnesium active in both tests did not affect locomotor activity. To evaluate the tolerance to these effects, we also performed experiments on the following acute/chronic magnesium treatment schedule: chronic saline and saline challenge at 0.5 h before behavioral experiments or serum magnesium determination (S+S), chronic saline and magnesium challenge (S+Mg), chronic magnesium and saline challenge (Mg+S), chronic magnesium and magnesium challenge (Mg+Mg). The antidepressant- and anxiolytic-like effect of magnesium was demonstrated in groups treated acutely and chronically with magnesium (Mg+Mg), but not in the Mg+S group. Moreover, these effects seem to be connected with at least 58% increase in serum magnesium concentration.
The results indicate that magnesium induces the antidepressant- and anxiolytic-like effects without tolerance to these activities, which suggests a potential antidepressant and anxiolytic activity of magnesium in these disorders in humans. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0091-3057 1873-5177 |
DOI: | 10.1016/j.pbb.2004.01.006 |