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Adult Tph2 knockout mice without brain serotonin have moderately elevated spine trabecular bone but moderately low cortical bone thickness.没有脑血清素的成年Tph2基因敲除小鼠的脊柱小梁骨适度增加，但皮质骨厚度适度降低。
Bonekey Rep. 2015 Jul 15;4:718. doi: 10.1038/bonekey.2015.87. eCollection 2015.
2
Genetic disruption of both tryptophan hydroxylase genes dramatically reduces serotonin and affects behavior in models sensitive to antidepressants.色氨酸羟化酶两个基因的遗传破坏会显著降低血清素水平，并影响对抗抑郁药敏感的模型中的行为。
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3
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4
Spatio-temporal expression of tryptophan hydroxylase isoforms in murine and human brain: convergent data from Tph2 knockout mice.色氨酸羟化酶亚型在小鼠和人脑中的时空表达：来自Tph2基因敲除小鼠的一致数据
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Differential tissue distribution of tryptophan hydroxylase isoforms 1 and 2 as revealed with monospecific antibodies.用单特异性抗体揭示色氨酸羟化酶同工型1和2的差异组织分布。
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[Abnormal cardiac activity in mice in the absence of peripheral serotonin synthesis].[外周5-羟色胺合成缺失小鼠的心脏活动异常]
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Peripartum dietary supplementation of a small-molecule inhibitor of tryptophan hydroxylase 1 compromises infant, but not maternal, bone.围产期补充色氨酸羟化酶 1 的小分子抑制剂会损害婴儿的骨骼，但不损害母亲的骨骼。
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本文引用的文献

1
High-throughput screening of mouse gene knockouts identifies established and novel skeletal phenotypes.高通量筛选小鼠基因敲除品系鉴定出已建立和新的骨骼表型。
Bone Res. 2014 Oct 28;2:14034. doi: 10.1038/boneres.2014.34. eCollection 2014.
2
Inhibiting peripheral serotonin synthesis reduces obesity and metabolic dysfunction by promoting brown adipose tissue thermogenesis.抑制外周血清素合成可通过促进棕色脂肪组织产热来减轻肥胖和代谢功能障碍。
Nat Med. 2015 Feb;21(2):166-72. doi: 10.1038/nm.3766. Epub 2014 Dec 8.
3
Reply to Lrp5 regulation of bone mass and gut serotonin synthesis.对Lrp5对骨量和肠道5-羟色胺合成的调节作用的回复。
Nat Med. 2014 Nov;20(11):1229-30. doi: 10.1038/nm.3697.
4
Life without brain serotonin: reevaluation of serotonin function with mice deficient in brain serotonin synthesis.缺乏脑血清素的生活：利用脑血清素合成缺陷小鼠对血清素功能的重新评估。
Behav Brain Res. 2015 Jan 15;277:78-88. doi: 10.1016/j.bbr.2014.06.005. Epub 2014 Jun 11.
5
Important role of mucosal serotonin in colonic propulsion and peristaltic reflexes: in vitro analyses in mice lacking tryptophan hydroxylase 1.黏膜 5-羟色胺在结肠推进和蠕动反射中的重要作用：缺乏色氨酸羟化酶 1 的小鼠的体外分析。
J Physiol. 2013 Dec 1;591(23):5939-57. doi: 10.1113/jphysiol.2013.256230. Epub 2013 Oct 14.
6
Serotonin: good or bad for bone.血清素：对骨骼有益还是有害。
Bonekey Rep. 2012 Jul 4;1:120. doi: 10.1038/bonekey.2012.120. eCollection 2012.
7
Serotonin and the regulation of mammalian energy balance.血清素与哺乳动物能量平衡的调节。
Front Neurosci. 2013 Mar 27;7:36. doi: 10.3389/fnins.2013.00036. eCollection 2013.
8
Postnatal growth defects in mice with constitutive depletion of central serotonin.中枢血清素持续耗竭的小鼠产后生长缺陷。
ACS Chem Neurosci. 2013 Jan 16;4(1):171-81. doi: 10.1021/cn300165x. Epub 2012 Dec 15.
9
Life without peripheral serotonin: insights from tryptophan hydroxylase 1 knockout mice reveal the existence of paracrine/autocrine serotonergic networks.没有外周 5-羟色胺的生命：色氨酸羟化酶 1 敲除小鼠的研究揭示了旁分泌/自分泌 5-羟色胺能网络的存在。
ACS Chem Neurosci. 2013 Jan 16;4(1):64-71. doi: 10.1021/cn300154j. Epub 2012 Nov 7.
10
Serotonin is a sword and a shield of the bowel: serotonin plays offense and defense.血清素是肠道的一把剑和一面盾：血清素兼具攻击和防御作用。
Trans Am Clin Climatol Assoc. 2012;123:268-80; discussion 280.

没有脑血清素的成年Tph2基因敲除小鼠的脊柱小梁骨适度增加，但皮质骨厚度适度降低。

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

作者信息

Brommage Robert, Liu Jeff, Doree Deon, Yu Wangsheng, Powell David R, Melissa Yang Qi

机构信息

Lexicon Pharmaceuticals , The Woodlands, TX, USA.

出版信息

Bonekey Rep. 2015 Jul 15;4:718. doi: 10.1038/bonekey.2015.87. eCollection 2015.

DOI:10.1038/bonekey.2015.87
PMID:26229596
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4516133/
Abstract

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.

摘要

据宣称，通过敲除小鼠色氨酸羟化酶基因（外周Tph1和神经元Tph2）来破坏神经元和外周的5-羟色胺合成，会导致骨量减少（Tph2基因敲除）和增加（Tph1基因敲除）。在本报告中，观察到成年雄性和雌性Tph2基因敲除小鼠的脊柱小梁骨增加。雌性Tph2基因敲除小鼠的股骨干中部皮质骨厚度减小。作为Tph1/Tph2双基因敲除（DKO）小鼠队列的一部分进行检测的雄性和雌性Tph1基因敲除小鼠的骨量正常。