Unknown

Dataset Information

0

Growth retardation and altered autonomic control in mice lacking brain serotonin.

ABSTRACT: Serotonin synthesis in mammals is initiated by 2 distinct tryptophan hydroxylases (TPH), TPH1 and TPH2. By genetically ablating TPH2, we created mice (Tph2(-/-)) that lack serotonin in the central nervous system. Surprisingly, these mice can be born and survive until adulthood. However, depletion of serotonin signaling in the brain leads to growth retardation and 50% lethality in the first 4 weeks of postnatal life. Telemetric monitoring revealed more extended daytime sleep, suppressed respiration, altered body temperature control, and decreased blood pressure (BP) and heart rate (HR) during nighttime in Tph2(-/-) mice. Moreover, Tph2(-/-) females, despite being fertile and producing milk, exhibit impaired maternal care leading to poor survival of their pups. These data confirm that the majority of central serotonin is generated by TPH2. TPH2-derived serotonin is involved in the regulation of behavior and autonomic pathways but is not essential for adult life.

SUBMITTER: Alenina N 

PROVIDER: S-EPMC2700938 | biostudies-literature | 2009 Jun

REPOSITORIES: biostudies-literature

Json Xml
altmetric image

Publications

Growth retardation and altered autonomic control in mice lacking brain serotonin.

Alenina Natalia N   Kikic Dana D   Todiras Mihail M   Mosienko Valentina V   Qadri Fatimunnisa F   Plehm Ralph R   Boyé Philipp P   Vilianovitch Larissa L   Sohr Reinhard R   Tenner Katja K   Hörtnagl Heide H   Bader Michael M  

Proceedings of the National Academy of Sciences of the United States of America 20090611 25

Serotonin synthesis in mammals is initiated by 2 distinct tryptophan hydroxylases (TPH), TPH1 and TPH2. By genetically ablating TPH2, we created mice (Tph2(-/-)) that lack serotonin in the central nervous system. Surprisingly, these mice can be born and survive until adulthood. However, depletion of serotonin signaling in the brain leads to growth retardation and 50% lethality in the first 4 weeks of postnatal life. Telemetric monitoring revealed more extended daytime sleep, suppressed respirati  ...[more]

Similar Datasets

Unknown SOCS-6 binds to insulin receptor substrate 4, and mice lacking the SOCS-6 gene exhibit mild growth retardation.
| S-EPMC133908 | biostudies-literature
Unknown Altered mRNA transport, docking, and protein translation in neurons lacking fragile X mental retardation protein.
| S-EPMC2932564 | biostudies-literature
Unknown Altered RNA editing in mice lacking ADAR2 autoregulation.
| S-EPMC1346902 | biostudies-literature
Unknown Severe growth retardation and early lethality in mice lacking the nuclear localization sequence and C-terminus of PTH-related protein.
| S-EPMC2629292 | biostudies-literature
Unknown Responses to chronic corticosterone on brain glucocorticoid receptors, adrenal gland, and gut microbiota in mice lacking neuronal serotonin.
| S-EPMC8650149 | biostudies-literature
Unknown Mice lacking full length Adgrb1 (Bai1) exhibit social deficits, increased seizure susceptibility, and altered brain development.
| S-EPMC9817291 | biostudies-literature
Unknown Mitochondrial brain proteome acetylation levels and behavioural responsiveness to amphetamine are altered in mice lacking Sirt3.
| S-EPMC9489219 | biostudies-literature
Unknown Growth retardation, impaired triacylglycerol catabolism, hepatic steatosis, and lethal skin barrier defect in mice lacking comparative gene identification-58 (CGI-58).
| S-EPMC2844178 | biostudies-literature
Unknown Altered palmitoylation and neuropathological deficits in mice lacking HIP14.
| S-EPMC3177655 | biostudies-literature
Unknown Brain injury induces specific changes in the caecal microbiota of mice via altered autonomic activity and mucoprotein production.
| S-EPMC5021180 | biostudies-literature