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Adult Tph2 knockout mice without brain serotonin have moderately elevated spine trabecular bone but moderately low cortical bone thickness

机译:没有脑5-羟色胺的成年Tph2基因敲除小鼠的脊柱小梁骨适度升高但皮质骨厚度适度低

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摘要

Disruption of serotonin synthesis in neurons and the periphery by knockout (KO) of mouse genes for tryptophan hydroxylases (peripheral Tph1 and neuronal Tph2) has been claimed to decrease (Tph2 KO) and increase (Tph1 KO) bone mass. In this report, adult male and female Tph2 KO mice were observed to have elevated spine trabecular bone. Female Tph2 KO mice have reduced midshaft femur cortical bone thickness. Bone mass was normal in male and female Tph1 KO mice examined as part of a Tph1/Tph2 double knockout (DKO) mouse cohort.
机译:据称色氨酸羟化酶的小鼠基因(外周Tph1和神经元Tph2)的基因敲除(KO)破坏了神经元和外周的血清素合成,从而减少(Tph2 KO)和增加(Tph1 KO)骨量。在此报告中,观察到成年雄性和雌性Tph2 KO小鼠的脊柱小梁骨升高。雌性Tph2 KO小鼠的股骨干中轴皮质骨厚度减少。作为Tph1 / Tph2双敲除(DKO)小鼠队列研究的一部分,雄性和雌性Tph1 KO小鼠的骨量正常。

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