Mosienko Valentina, Beis Daniel, Pasqualetti Massimo, Waider Jonas, Matthes Susann, Qadri Fatimunnisa, Bader Michael, Alenina Natalia
Max-Delbrueck-Center for Molecular Medicine, Berlin, Germany.
Department of Biology, Unit of Cell and Developmental Biology, University of Pisa, Pisa, Italy.
Behav Brain Res. 2015 Jan 15;277:78-88. doi: 10.1016/j.bbr.2014.06.005. Epub 2014 Jun 11.
Tryptophan hydroxylase (TPH) is a rate limiting enzyme in the synthesis of serotonin (5-HT), a monoamine which works as an autacoid in the periphery and as a neurotransmitter in the central nervous system. In 2003 we have discovered the existence of a second Tph gene, which is expressed exclusively in the brain, and, therefore, is responsible for the 5-HT synthesis in the central nervous system. In the following years several research groups have independently generated Tph2-deficient mice. In this review we will summarize the data gained from the existing mouse models with constitutive or conditional deletion of the Tph2 gene, focusing on biochemical, developmental, and behavioral consequences of Tph2-deficiency.
色氨酸羟化酶（TPH）是血清素（5-羟色胺，5-HT）合成中的限速酶，5-羟色胺是一种单胺类物质，在外周作为自分泌调节物质起作用，在中枢神经系统中作为神经递质起作用。2003年，我们发现了第二个Tph基因的存在，该基因仅在大脑中表达，因此负责中枢神经系统中5-羟色胺的合成。在接下来的几年里，几个研究小组独立培育出了Tph2基因缺陷小鼠。在这篇综述中，我们将总结从现有组成型或条件性缺失Tph2基因的小鼠模型中获得的数据，重点关注Tph2基因缺陷的生化、发育和行为后果。
