GPR39 up-regulation after selective antidepressants

Recent studies indicated that zinc activates neural transmission via the GPR39 Zn2+-sensing receptor. Preclinical and clinical studies demonstrated the antidepressant properties of zinc. To investigate whether the GPR39 receptor is involved in the mechanism of antidepressant action, we measured the...

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Bibliographic Details
Published inNeurochemistry international Vol. 62; no. 7; pp. 936 - 939
Main Authors Młyniec, Katarzyna, Nowak, Gabriel
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.06.2013
Subjects
Animals
Antidepressants
Antidepressive Agents - pharmacology
Brain - metabolism
Bupropion - pharmacology
Citalopram - pharmacology
Depression
GPR39
Imipramine - pharmacology
Male
Mice
Morpholines - pharmacology
Receptors, G-Protein-Coupled - metabolism
Up-Regulation - drug effects
Zinc
Zinc - metabolism
Zn2+-Sensing receptor
GPR39
Depression
Zn2+-Sensing receptor
Antidepressants
Zinc
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Summary:Recent studies indicated that zinc activates neural transmission via the GPR39 Zn2+-sensing receptor. Preclinical and clinical studies demonstrated the antidepressant properties of zinc. To investigate whether the GPR39 receptor is involved in the mechanism of antidepressant action, we measured the expression of the GPR39 receptor (Western Blot) in the frontal cortex of mice treated intraperitoneally with imipramine (30mg/kg), escitalopram (4mg/kg), reboxetine (10mg/kg) or bupropion (15mg/kg) for 14days. The present study shows the up-regulation of the GPR39 receptor protein level after escitalopram (by 290%), reboxetine (by 816%) and bupropion (by 272%), but not imipramine treatment. This is the first report to indicate the involvement of the GPR39 Zn2+-sensing receptor in the antidepressant effect of selective monoamine reuptake inhibitors.
ISSN:0197-0186
1872-9754
DOI:10.1016/j.neuint.2013.02.024