Do Limits of Neuronal Plasticity Represent an Opportunity for Mental Diseases, Such as Addiction to Food and Illegal Drugs? Use and Utilities of Serotonin Receptor Knock-Out Mice

2007 ◽  
pp. 157-180 ◽  
Author(s):  
Valerie Compan
Keyword(s):  
Neuronal Plasticity ◽  
Serotonin Receptor ◽  
Illegal Drugs ◽  
Knock Out ◽  
Mental Diseases ◽  
Knock Out Mice

3-Iodothyronamine Induces Diverse Signaling Effects at Different Aminergic and Non-Aminergic G-Protein Coupled Receptors

2019 ◽  
Vol 128 (06/07) ◽  
pp. 395-400 ◽  
Author(s):  
Heike Biebermann ◽  
Gunnar Kleinau
Keyword(s):  
Body Temperature ◽  
G Protein ◽  
Intracellular Signaling ◽  
Serotonin Receptor ◽  
Fine Tuning ◽  
Specific Cell ◽  
Knock Out ◽  
Alpha2 Adrenoceptor ◽  
Knock Out Mice ◽  
G Protein Coupled

AbstractThe thyroid hormone metabolite 3-iodothyronamine (3-T1AM) exerts diverse physiological reactions such as a decrease of body temperature, and negative inotropic and chronotropic effects. This observed pleomorphic effect in physiology can be barely explained by interaction with only one target protein such as the trace-amine receptor 1 (TAAR1), a class A G-protein coupled receptor (GPCR). Moreover, Taar1 knock-out mice still react to 3-T1AM through physiological responses with a rapid decrease in body temperature. These facts propelled our group and others to search for further targets for this molecule.The group of TAARs evolved early in evolution and, according to sequence similarities, they are closely related to adrenoceptors and other aminergic receptors. Therefore, several of these receptors were characterized by their potential to interplay with 3-T1AM. Indeed, 3-T1AM acts as a positive allosteric modulator on the beta2-adrenoceptor (ADRB2) and as a biased agonist on the serotonin receptor 1B (5HT1b) and the alpha2-adrenoceptor (ADRA2A). In addition, 3-T1AM was reported to be a weak antagonist at a non-aminergic muscarinic receptor (M3).These findings impressively reflect that such trace amines can unselectively and simultaneously function at different receptors expressed by one cell or at different tissues. In conclusion, the role of 3-T1AM is hypothesized to concert the fine-tuning of specific cell reactions by the accentuation of certain pathways dependent on distinct receptors. 3-T1AM acts as a regulator of signals by blocking, modulating, or inducing simultaneously distinct intracellular signaling cascades via different GPCRs.

scholarly journals Gene expression and mRNA editing of serotonin receptor 2C in brains of HPRT gene knock-out mice, an animal model of Lesch-Nyhan disease

2009 ◽  
Vol 16 (8) ◽  
pp. 1061-1063 ◽  
Author(s):  
Matteo Bertelli ◽  
Brunilda Alushi ◽  
Arsenio Veicsteinas ◽  
H.A. Jinnah ◽  
Vanna Micheli
Keyword(s):  
Gene Expression ◽  
Animal Model ◽  
Serotonin Receptor ◽  
Hprt Gene ◽  
Mrna Editing ◽  
Knock Out ◽  
Knock Out Mice

Increased glyoxalase-1 levels in Fkbp5 knock-out mice caused by Glo1 gene duplication

2013 ◽  
Vol 46 (06) ◽  
Author(s):  
LK Kollmannsberger ◽  
NC Gassen ◽  
A Bultmann ◽  
J Hartmann ◽  
P Weber ◽  
...  
Keyword(s):  
Gene Duplication ◽  
Knock Out ◽  
Glyoxalase 1 ◽  
Knock Out Mice

Functional characterization of the H+/K+ ATPase in wild type and gastrin knock-out mice

2007 ◽  
Vol 45 (05) ◽  
Author(s):  
A Schnur ◽  
P Hegyi ◽  
V Venglovecz ◽  
Z Rakonczay ◽  
I Ignáth ◽  
...  
Keyword(s):  
Functional Characterization ◽  
Wild Type ◽  
Knock Out ◽  
Knock Out Mice

Nr4a1 and Nr4a3 Knock Out Mice Have Impaired Glucose Clearance and Beta-Cell Function under High-Fat Feeding

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2040-P
Author(s):  
COURTNEY J. SMITH ◽  
KYLE B. KENER ◽  
JEFFERY S. TESSEM
Keyword(s):  
Beta Cell ◽  
Beta Cell Function ◽  
Cell Function ◽  
High Fat ◽  
Knock Out ◽  
Glucose Clearance ◽  
Knock Out Mice ◽  
Fat Feeding
Sign in / Sign up

Export Citation Format

Share Document