scholarly journals Brain serotonin deficiency leads to social communication deficits in mice

2015 ◽  
Vol 11 (3) ◽  
pp. 20150057 ◽  
Author(s):  
D. Beis ◽  
K. Holzwarth ◽  
M. Flinders ◽  
M. Bader ◽  
M. Wöhr ◽  
...  
Keyword(s):  
Tryptophan Hydroxylase ◽  
Sexual Preference ◽  
Brain Serotonin ◽  
Adult Males ◽  
Social Situations ◽  
Tryptophan Hydroxylase 2 ◽  
Social Contacts ◽  
Interaction Partners ◽  
Female Urine ◽  
Serotonin Deficiency

A deficit in brain serotonin is thought to be associated with deteriorated stress coping behaviour, affective disorders and exaggerated violence. We challenged this hypothesis in mice with a brain-specific serotonin depletion caused by a tryptophan hydroxylase 2 (TPH2) deficiency. We tested TPH2-deficient ( Tph2 −/– ) animals in two social situations. As juveniles, Tph2 −/− mice displayed reduced social contacts, whereas ultrasonic vocalizations (USVs) were unchanged within same-sex same-genotype pairings. Interestingly, juvenile females vocalized more than males across genotypes. Sexually naive adult males were exposed to fresh male or female urine, followed by an interaction with a conspecific, and re-exposed to urine. Although Tph2 −/− mice showed normal sexual preference, they were hyper-aggressive towards their interaction partners and did not vocalize in response to sexual cues. These results highlight that central serotonin is essential for prosocial behaviour, especially USV production in adulthood, but not for sexual preference.

Targeted Manipulation of Brain Serotonin: RNAi-Mediated Knockdown of Tryptophan Hydroxylase 2 in Rats

2019 ◽  
Vol 10 (7) ◽  
pp. 3207-3217 ◽  
Author(s):  
Susann Matthes ◽  
Valentina Mosienko ◽  
Elena Popova ◽  
Marion Rivalan ◽  
Michael Bader ◽  
...  
Keyword(s):  
Tryptophan Hydroxylase ◽  
Brain Serotonin ◽  
Tryptophan Hydroxylase 2

The Combined Effects of Amyloidosis and Serotonin Deficiency by Tryptophan Hydroxylase-2 Knockout Impacts Viability of the APP/PS1 Mouse Model of Alzheimer’s Disease

2021 ◽  
pp. 1-18
Author(s):  
Christian Ulrich von Linstow ◽  
Jonas Waider ◽  
Marianne Skov-Skov Bergh ◽  
Marco Anzalone ◽  
Cecilie Madsen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tryptophan Hydroxylase ◽  
Presenilin 1 ◽  
Mrna Levels ◽  
Combined Effects ◽  
Tryptophan Hydroxylase 2 ◽  
Model Of Alzheimer’S Disease ◽  
Serotonin Deficiency ◽  
Targeted Inactivation

Background: A decline of brain serotonin (5-HT) is held responsible for the changes in mood that can be observed in Alzheimer’s disease (AD). However, 5-HT’ergic signaling is also suggested to reduce the production of pathogenic amyloid-4β (Aβ). Objective: To investigate the effect of targeted inactivation of tryptophan hydroxylase-2 (Tph2), which is essential for neuronal 5-HT synthesis, on amyloidosis in amyloid precursor protein (APP)swe/presenilin 1 (PS1) ΔE9 transgenic mice. Methods: Triple-transgenic (3xTg) APP/PS1 mice with partial (+/-) or complete Tph2 knockout (–/–) were allowed to survive until 6 months old with APP/PS1, Tph2–/–, and wildtype mice. Survival and weight were recorded. Levels of Aβ 42/40/38, soluble APPα (sAβPPα) and sAβPPβ, and cytokines were analyzed by mesoscale, neurotransmitters by mass spectrometry, and gene expression by quantitative PCR. Tph2, microglia, and Aβ were visualized histologically. Results: Tph2 inactivation in APP/PS1 mice significantly reduced viability, without impacting soluble and insoluble Aβ 42 and Aβ 40 in neocortex and hippocampus, and with only mild changes of soluble Aβ 42/Aβ 40. However, sAβPPα and sAβPPβ in hippocampus and Aβ 38 and Aβ 40 in cerebrospinal fluid were reduced. 3xTg–/–mice were devoid of Tph2 immunopositive fibers and 5-HT. Cytokines were unaffected by genotype, as were neocortical TNF, HTR2a and HTR2b mRNA levels in Tph2–/– mice. Microglia clustered around Aβ plaques regardless of genotype. Conclusion: The results suggest that Tph2 inactivation influences AβPP processing, at least in the hippocampus, although levels of Aβ are unchanged. The reduced viability of 3xTg–/–mice could indicate that 5-HT protects against the seizures that can impact the viability of APP/PS1 mice.

scholarly journals Tryptophan hydroxylase 2 genotype determines brain serotonin synthesis but not tissue content in C57Bl/6 and BALB/c congenic mice

2010 ◽  
Vol 481 (1) ◽  
pp. 6-11 ◽  
Author(s):  
William B. Siesser ◽  
Xiaodong Zhang ◽  
Jacob P.R. Jacobsen ◽  
Tatyana D. Sotnikova ◽  
Raul R. Gainetdinov ◽  
...  
Keyword(s):  
Tryptophan Hydroxylase ◽  
Brain Serotonin ◽  
Serotonin Synthesis ◽  
Tryptophan Hydroxylase 2 ◽  
Congenic Mice ◽  
Tissue Content

scholarly journals The Intricate Biological Proximity of Vitamin D and Brain Serotonin

2021 ◽  
Vol 9 (12) ◽  
pp. 2096-2099
Author(s):  
Abhineet Maini
Keyword(s):  
Vitamin D ◽  
Clinical Trials ◽  
Tryptophan Hydroxylase ◽  
Current Understanding ◽  
Brain Serotonin ◽  
Autistic Children ◽  
Serotonin Synthesis ◽  
Tryptophan Hydroxylase 2

Abstract: Background: The purpose of this article is to extend and elaborate on our current understanding of Calcitriol and Brain Serotonin synthesis; particularly on how the two may be related. Methods: Using a 2014 study involving clinical trials to extend this hypothesis. Results: Vitamin D (Calcitriol) activated the gene that codes for Tryptophan Hydroxylase 2, which synthesizes Brain Serotonin. It also inhibits Tryptophan Hydroxylase 1, which makes serotonin in the gut. Conclusion: Vitamin D is closely related to the synthesis of Brain Serotonin. If furthered, it may be used as a treatment for the Serotonin Anomaly in Autistic Children. Keywords: 1. Biochemistry 2. Genetics 3. Neuroscience 4. Physiology

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