scholarly journals Histidine Decarboxylase Knockout Mice as a Model of the Pathophysiology of Tourette Syndrome and Related Conditions

Author(s):  
Christopher Pittenger

2015 ◽  
Vol 595 ◽  
pp. 50-53 ◽  
Author(s):  
Meiyu Xu ◽  
Lina Li ◽  
Hiroshi Ohtsu ◽  
Christopher Pittenger


2005 ◽  
Vol 522 (1-3) ◽  
pp. 55-62 ◽  
Author(s):  
Akiko Yoshida ◽  
Jalal Izadi Mobarakeh ◽  
Eiko Sakurai ◽  
Shinobu Sakurada ◽  
Tohru Orito ◽  
...  


FEBS Letters ◽  
2001 ◽  
Vol 508 (2) ◽  
pp. 245-248 ◽  
Author(s):  
Carlos P. Fitzsimons ◽  
Eszter Lazar-Molnar ◽  
Zsuzsa Tomoskozi ◽  
Edit Buzás ◽  
Elena S. Rivera ◽  
...  




2012 ◽  
Vol 3 (2) ◽  
Author(s):  
Ruben Cauchi ◽  
Zsanett Tárnok

AbstractTourette syndrome (TS) is a disabling neuropsychiatric disorder characterised by persistent motor and vocal tics. TS is a highly comorbid state, hence, patients might experience anxiety, obsessions, compulsions, sleep abnormalities, depression, emotional liability, learning problems, and attention deficits in addition to tics. In spite of its complex heterogeneous genetic aetiology, recent studies highlighted a strong link between TS and genetic lesions in the HDC (L-histidine decarboxylase) gene, which encodes the enzyme that synthetises histamine, and the SLITRK1 (SLIT and TRK-like family member 1) gene, which encodes a transmembrane protein that was found to regulate neurite outgrowth. In addition to validating the contribution of a specific genetic aberration to the development of a particular pathology, animal models are crucial to dissect the function of disease-linked proteins, expose disease pathways through examination of genetic modifiers and discover as well as assess therapeutic strategies. Mice with a knockout of either Hdc or Slitrk1 exhibit anxiety and those lacking Hdc, display dopamine agonist-triggered stereotypic movements. However, the mouse knockouts do not spontaneously display tics, which are recognised as the hallmark of TS. In this review, we explore the features of the present genetic animal models of TS and identify reasons for their poor resemblance to the human condition. Importantly, we highlight ways forward aimed at developing a valuable genetic model of TS or a model that has good predictive validity in developing therapeutic drugs for the treatment of tics, hence potentially accelerating the arduous journey from lab to clinic.



SLEEP ◽  
2019 ◽  
Vol 42 (5) ◽  
Author(s):  
Xiao Yu ◽  
Ying Ma ◽  
Edward C Harding ◽  
Raquel Yustos ◽  
Alexei L Vyssotski ◽  
...  

Abstract Acute chemogenetic inhibition of histamine (HA) neurons in adult mice induced nonrapid eye movement (NREM) sleep with an increased delta power. By contrast, selective genetic lesioning of HA neurons with caspase in adult mice exhibited a normal sleep–wake cycle overall, except at the diurnal start of the lights-off period, when they remained sleepier. The amount of time spent in NREM sleep and in the wake state in mice with lesioned HA neurons was unchanged over 24 hr, but the sleep–wake cycle was more fragmented. Both the delayed increase in wakefulness at the start of the night and the sleep–wake fragmentation are similar phenotypes to histidine decarboxylase knockout mice, which cannot synthesize HA. Chronic loss of HA neurons did not affect sleep homeostasis after sleep deprivation. However, the chronic loss of HA neurons or chemogenetic inhibition of HA neurons did notably reduce the ability of the wake-promoting compound modafinil to sustain wakefulness. Thus, part of modafinil’s wake-promoting actions arise through the HA system.



2007 ◽  
Vol 179 (10) ◽  
pp. 6613-6619 ◽  
Author(s):  
Agnes Koncz ◽  
Maria Pasztoi ◽  
Mercedesz Mazan ◽  
Ferenc Fazakas ◽  
Edit Buzas ◽  
...  


Neuron ◽  
2014 ◽  
Vol 81 (1) ◽  
pp. 77-90 ◽  
Author(s):  
Lissandra Castellan Baldan ◽  
Kyle A. Williams ◽  
Jean-Dominique Gallezot ◽  
Vladimir Pogorelov ◽  
Maximiliano Rapanelli ◽  
...  


2005 ◽  
Vol 14 (3) ◽  
pp. 169-175 ◽  
Author(s):  
M. Seike ◽  
M. Ikeda ◽  
H. Kodama ◽  
T. Terui ◽  
H. Ohtsu


2010 ◽  
Vol 48 (5) ◽  
pp. 727-735 ◽  
Author(s):  
Yao Shen ◽  
Ping He ◽  
Yan-ying Fan ◽  
Jian-xiang Zhang ◽  
Hai-jing Yan ◽  
...  


Sign in / Sign up

Export Citation Format

Share Document