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Minocycline increases phosphorylation and membrane insertion of neuronal GluR1 receptors.

机译:米诺环素增加神经元GluR1受体的磷酸化和膜插入。

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摘要

The tetracycline antibiotic minocycline beneficially affects neuronal functioning and also inhibits the enzyme 5-lipoxygenase (5-LOX). We hypothesized that similar to 5-LOX inhibitors, minocycline may increase phosphorylation and membrane insertion of the glutamate receptor GluR1. The experiments were performed in primary cultures of mouse striatal neurons and in the prefrontal cortex and striatum of minocycline-treated mice. In vitro, low micromolar minocycline concentrations increased GluR1 phosphorylation at Ser845 and Ser831 and increased the surface content of GluR1. Minocycline also increased GluR1 phosphorylation in vivo. Increased GluR1 phosphorylation and minocycline treatment have been associated with antidepressant and memory-enhancing activities. Direct consequences of minocycline-increased GluR1 phosphorylation are yet to be established.
机译:四环素抗生素米诺环素有益地影响神经元功能,还抑制5-脂氧合酶(5-LOX)。我们假设与5-LOX抑制剂相似,米诺环素可能会增加谷氨酸受体GluR1的磷酸化和膜插入。实验是在小鼠纹状体神经元的原代培养物中以及在米诺环素治疗的小鼠的前额叶皮层和纹状体中进行的。在体外,低摩尔浓度的米诺环素会增加Ser845和Ser831处的GluR1磷酸化,并增加GluR1的表面含量。米诺环素还增加了体内的GluR1磷酸化。增加的GluR1磷酸化和米诺环素治疗与抗抑郁药和增强记忆力有关。米诺环素增加的GluR1磷酸化的直接后果尚未确定。

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