scholarly journals Role of the novel tryptophan hydroxylase-2 gene in Tourette syndrome

2007 ◽  
Vol 12 (7) ◽  
pp. 617-619 ◽  
Author(s):  
R Mössner ◽  
K R Müller-Vahl ◽  
N Döring ◽  
M Stuhrmann
Keyword(s):  
Tourette Syndrome ◽  
Tryptophan Hydroxylase ◽  
The Novel ◽  
Tryptophan Hydroxylase 2

scholarly journals ROLE OF THE ALLELIC VARIATION IN THE 5-HYDROXYTRYPTAMINE RECEPTOR 1A (HTR1A) AND THE TRYPTOPHAN HYDROXYLASE 2 (TPH2) GENES IN THE DEVELOPMENT OF PTSD

2019 ◽  
Vol 31 (2) ◽  
pp. 256-262 ◽  
Author(s):  
Aferdita Goci Uka ◽  
◽  
Ferid Agani ◽  
Afrim Blyta ◽  
Blerina Hoxha ◽  
...  
Keyword(s):  
Tryptophan Hydroxylase ◽  
Allelic Variation ◽  
Tryptophan Hydroxylase 2

Time- and age-dependent effects of serotonin on gasping and autoresuscitation in neonatal mice

2013 ◽  
Vol 114 (12) ◽  
pp. 1668-1676 ◽  
Author(s):  
Jianping Chen ◽  
Jennifer Magnusson ◽  
Gerard Karsenty ◽  
Kevin J. Cummings
Keyword(s):  
Heart Rate ◽  
Tryptophan Hydroxylase ◽  
Single Injection ◽  
Heart Rate Recovery ◽  
Wild Type ◽  
Tryptophan Hydroxylase 2 ◽  
Age Dependent ◽  
Long Time ◽  
Time Required

The role of brain stem serotonin (5-hydroxytryptamine, 5-HT) in autoresuscitation in neonatal life is unclear. We hypothesized that a specific loss of 5-HT would compromise gasping and autoresuscitation mainly in the second postnatal week and that acute restoration of 5-HT would reverse the defects. We exposed postnatal day (P)4–5, P8–9, and P11–12 tryptophan-hydroxylase-2 knockout ( TPH2−/−) and wild-type littermates (WT) to 10 episodes of anoxia (97% N2, 3% CO2), measuring survival, gasp latency, gasp frequency ( fB), and the time required to restore eupnea and heart rate. We also tested P8–9 TPH2−/− mice after restoring 5-HT with a single injection of 5-hydroxytryptophan (5-HTP) 1–2 h before testing or with multiple injections beginning 24 h before testing. At P4–5 and P8–9, but not at P11–12, gasp latency and the recovery of eupnea were delayed ∼2- to 3-fold in TPH2−/− pups compared with WT ( P < 0.001). At all ages, TPH2−/− pups displayed reduced gasp fB (∼20–30%; P < 0.001) and delayed heart rate recovery (∼60%; P = 0.002) compared with WT littermates. TPH2−/− survival was reduced compared with WT ( P < 0.001), especially at P8–9 and P11–12 ( P = 0.004). Whereas 1–2 h of 5-HTP treatment improved the gasp latency and fB of P8–9 TPH2−/− pups, improved cardiorespiratory recovery and survival required 24 h of treatment. Our data suggest that 5-HT operates over a long time span (∼24 h) to improve survival during episodic severe hypoxia. Early in development (P4–9), 5-HT is critical for both respiratory and cardiovascular components of autoresuscitation; later (P11–12), it is critical mainly for cardiovascular components. Nevertheless, the effect of 5-HT deficiency on survival is most striking from P8 to P12.

The novel brain-specific tryptophan hydroxylase-2 gene in panic disorder

2006 ◽  
Vol 20 (4) ◽  
pp. 547-552 ◽  
Author(s):  
Rainald Mössner ◽  
Christine M. Freitag ◽  
Lise Gutknecht ◽  
Andreas Reif ◽  
Ralf Tauber ◽  
...  
Keyword(s):  
Panic Disorder ◽  
Tryptophan Hydroxylase ◽  
The Novel ◽  
Tryptophan Hydroxylase 2

scholarly journals The 5-HT deficiency theory of depression: perspectives from a naturalistic 5-HT deficiency model, the tryptophan hydroxylase 2 Arg 439 His knockin mouse

2012 ◽  
Vol 367 (1601) ◽  
pp. 2444-2459 ◽  
Author(s):  
Jacob P. R. Jacobsen ◽  
Ivan O. Medvedev ◽  
Marc G. Caron
Keyword(s):  
Tryptophan Hydroxylase ◽  
Tryptophan Hydroxylase 2 ◽  
The Past ◽  
Clinical Observations ◽  
Antidepressant Effects ◽  
Tph2 Gene ◽  
Primary Deficit ◽  
Suicidal Patients ◽  
Knockin Mouse

A decreased level of brain 5-hydroxytryptamine (5-HT) has been theorized to be a core pathogenic factor in depression for half a century. The theory arose from clinical observations that drugs enhancing extracellular levels of 5-HT (5-HT Ext ) have antidepressant effects in many patients. However, whether such drugs indeed correct a primary deficit remains unresolved. Still, a number of anomalies in putative biomarkers of central 5-HT function have been repeatedly reported in depression patients over the past 40 years, collectively indicating that 5-HT deficiency could be present in depression, particularly in severely ill and/or suicidal patients. This body of literature on putative 5-HT biomarker anomalies and depression has recently been corroborated by data demonstrating that such anomalies indeed occur consequent to severely reduced 5-HT Ext levels in a mouse model of naturalistic 5-HT deficiency, the tryptophan hydroxylase 2 His 439 knockin (Tph2KI) mouse. In this review, we will critically assess the evidence for 5-HT deficiency in depression and the possible role of polymorphisms in the Tph2 gene as a causal factor in 5-HT deficiency, the latter investigated from a clinical as well as preclinical angle.

Impaired Executive Control Is Associated with a Variation in the Promoter Region of the Tryptophan Hydroxylase 2 Gene

2007 ◽  
Vol 19 (3) ◽  
pp. 401-408 ◽  
Author(s):  
Martin Reuter ◽  
Ulrich Ott ◽  
Dieter Vaitl ◽  
Jürgen Hennig
Keyword(s):  
Executive Control ◽  
Tryptophan Hydroxylase ◽  
Molecular Genetic ◽  
Twin Studies ◽  
Promoter Polymorphism ◽  
Tryptophan Hydroxylase 2 ◽  
Molecular Genetic Basis ◽  
Tph2 Gene ◽  
Attention Performance

Current models of attention describe attention not as a homogenous entity but as a set of neural networks whose measurement yields a set of three endophenotypes—alerting, orienting, and executive control. Previous findings revealed different neuroanatomical regions for these subsystems, and data from twin studies indicate differences in their heritability. The present study investigated the molecular genetic basis of attention in a sample of 100 healthy subjects. Attention performance was assessed with the attention network test that distinguishes alerting, orienting, and executive control (conflict) using a simple reaction time paradigm with different cues and congruent and incongruent flankers. Two gene loci on candidate genes for cognitive functioning, the functional catechol-O-methyltransferase (COMT) VAL158MET and the tryptophan hydroxylase 2 (TPH2) −703 G/T promoter polymorphism, were tested for possible associations with attention. COMT is involved in the catabolism of dopamine, and TPH is the rate-limiting enzyme for serotonin synthesis. Results showed no effect of the COMT polymorphism on attention performance. However, the TT genotype of TPH2 −03 G/T was significantly associated with more errors (a possible indicator of impaired impulse control; p = .001) and with decreased performance in executive control (p = .001). This single-nucleotide polymorphism on the TPH2 gene explained more than 10% of the variance in both indicators of attention stressing the role of the serotonergic system for cognitive functions.

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