Department of Biochemical Toxicology, Jagiellonian University Medical College, Medyczna 9, PL 30-688 Kraków, Poland.
Neurochem Int. 2013 Jun;62(7):936-9. doi: 10.1016/j.neuint.2013.02.024. Epub 2013 Mar 5.
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 (30 mg/kg), escitalopram (4 mg/kg), reboxetine (10 mg/kg) or bupropion (15 mg/kg) for 14 days. 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.
最近的研究表明，锌通过 GPR39 Zn²⁺感应受体激活神经传递。临床前和临床研究表明锌具有抗抑郁作用。为了研究 GPR39 受体是否参与抗抑郁作用的机制，我们测量了腹腔注射丙咪嗪（30mg/kg）、依地普仑（4mg/kg）、瑞波西汀（10mg/kg）或安非他酮（15mg/kg）14 天后，小鼠前额皮质中 GPR39 受体的表达（Western Blot）。本研究表明，依地普仑（增加 290%）、瑞波西汀（增加 816%）和安非他酮（增加 272%）处理后 GPR39 受体蛋白水平上调，但丙咪嗪处理则没有。这是第一项表明 GPR39 Zn²⁺感应受体参与选择性单胺再摄取抑制剂抗抑郁作用的报告。
