Brain-specific conditional and time-specific inducible Tph2 knockout mice possess normal serotonergic gene expression in the absence of serotonin during adult life

Kriegebaum, C.; Song, Ning‐Ning; Gutknecht, Lise; Huang, Ying; Schmitt, Angelika; Reif, Andreas; Ding, Yu; Lesch, Klaus‐Peter

doi:10.1016/j.neuint.2010.06.015

Cited by 41 publications

(35 citation statements)

References 22 publications

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“…6 K). This result agreed with a previous study showing no compensatory up-regulation of Tph1 in a tph2 knockout mouse (Kriegebaum et al, 2010). The AGMs were treated with AKT inhibitor at 10 µm, and then, the number of colonies in the CFU-C assay was counted, and the expression of runx1 and gfi1 was detected by qPCR analysis.…”

Section: Up-regulated Pet1-erk Signaling Promotes Hspc Proliferation supporting

confidence: 92%

5-hydroxytryptamine synthesized in the aorta-gonad-mesonephros regulates hematopoietic stem and progenitor cell survival

Wang

Liu

2017

Mechanisms of Development

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Section: Up-regulated Pet1-erk Signaling Promotes Hspc Proliferation supporting

confidence: 92%

5-hydroxytryptamine synthesized in the aorta-gonad-mesonephros regulates hematopoietic stem and progenitor cell survival

Wang

Liu

2017

Mechanisms of Development

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“…Notably, however, a consistent finding is that, despite almost complete lack of 5-HT, they show no overt changes in physical morphology, brain structure, neuron formation or fibre distribution. 33,[89][90][91][92] The observations of no overt morphological changes in rodents born with a 5-HT deficiency are at odds with the idea of the crucial role of 5-HT for further brain development. The lack of findings might be attributed to different factors, all of which may interact.…”

Section: Targeting Specific 5-ht Moleculesmentioning

confidence: 99%

Genetic and early environmental influences on the serotonin system: consequences for brain development and risk for psychopathology

Booij

Tremblay

Szyf

et al. 2015

jpn

107

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“…Tryptophan hydroxylase (Tph2) is the key enzyme for 5-HT synthesis in the brain (Zhang et al, 2004), and specific deletion of Tph2 leads to the central 5-HT deficiency without affecting the survival of the serotonergic neurons (Savelieva et al, 2008; Kriegebaum et al, 2010). The prototypical serotonergic transcription factor Pet1 is expressed in both central serotonergic neurons and pancreatic islet cells (Hendricks et al, 1999, 2003; Ohta et al, 2011), and Pet1 -driven Cre expression was used to simultaneously deplete these two kinds of cells in Pet1 -Cre;Rosa26-diphtheria toxin receptor (DTR) mice in adulthood.…”

Section: Introductionmentioning

confidence: 99%

Abnormal anxiety- and depression-like behaviors in mice lacking both central serotonergic neurons and pancreatic islet cells

Jia

Song

Mao

et al. 2014

Front. Behav. Neurosci.

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Dysfunction of central serotonin (5-HT) system has been proposed to be one of the underlying mechanisms for anxiety and depression, and the association of diabetes mellitus and psychiatric disorders has been noticed by the high prevalence of anxiety/depression in patients with diabetes mellitus. This promoted us to examine these behaviors in central 5-HT-deficient mice and those also suffering with diabetes mellitus. Mice lacking either 5-HT or central serotonergic neurons were generated by conditional deletion of Tph2 or Lmx1b respectively. Simultaneous depletion of both central serotonergic neurons and pancreatic islet cells was achieved by administration of diphtheria toxin (DT) in Pet1-Cre;Rosa26-DT receptor (DTR) mice. The central 5-HT-deficient mice showed reduced anxiety-like behaviors as they spent more time in and entered more often into the light box in the light/dark box test compared with controls; similar results were observed in the elevated plus maze test. However, they displayed no differences in the immobility time of the forced swimming and tail suspension tests suggesting normal depression-like behaviors in central 5-HT-deficient mice. As expected, DT-treated Pet1-Cre;Rosa26-DTR mice lacking both central serotonergic neurons and pancreatic islet endocrine cells exhibited several classic diabetic symptoms. Interestingly, they displayed increased anxiety-like behaviors but reduced immobility time in the forced swimming and tail suspension tests. Furthermore, the hippocampal neurogenesis was dramatically enhanced in these mice. These results suggest that the deficiency of central 5-HT may not be sufficient to induce anxiety/depression-like behaviors in mice, and the enhanced hippocampal neurogenesis may contribute to the altered depression-like behaviors in the 5-HT-deficient mice with diabetes. Our current investigation provides understanding the relationship between diabetes mellitus and psychiatric disorders.

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Brain-specific conditional and time-specific inducible Tph2 knockout mice possess normal serotonergic gene expression in the absence of serotonin during adult life

Cited by 41 publications

References 22 publications

5-hydroxytryptamine synthesized in the aorta-gonad-mesonephros regulates hematopoietic stem and progenitor cell survival

5-hydroxytryptamine synthesized in the aorta-gonad-mesonephros regulates hematopoietic stem and progenitor cell survival

Genetic and early environmental influences on the serotonin system: consequences for brain development and risk for psychopathology

Abnormal anxiety- and depression-like behaviors in mice lacking both central serotonergic neurons and pancreatic islet cells

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