scholarly journals Development of repetitive behavior in a mouse model: Roles of indirect and striosomal basal ganglia pathways

2011 ◽  
Vol 29 (4) ◽  
pp. 461-467 ◽  
Author(s):  
Yoko Tanimura ◽  
Michael A. King ◽  
Dustin K. Williams ◽  
Mark H. Lewis
Keyword(s):  
Basal Ganglia ◽  
Mouse Model ◽  
Repetitive Behavior

Spotlight on a mouse model of obsessive-compulsive disorder

2013 ◽  
Vol 28 (S2) ◽  
pp. 17-17
Author(s):  
E. Burguière
Keyword(s):  
Basal Ganglia ◽  
Mouse Model ◽  
Obsessive Compulsive Disorder ◽  
Response Inhibition ◽  
Mutant Mouse ◽  
Repetitive Behavior ◽  
Inhibitory Neurons ◽  
Obsessive Compulsive ◽  
Repetitive Behaviour ◽  
Compulsive Disorder

It has been shown these last years that optogenetic tool, that uses a combination of optics and genetics technics to control neuronal activity with light on behaving animals, allows to establish causal relationship between brain activity and normal or pathological behaviors [3]. In combination with animal model of neuropsychiatric disorder, optogenetic could help to identify deficient circuitry in numerous pathologies by exploring functional connectivity, with a specificity never reached before, while observing behavioral and/or physiological correlates. To illustrate the promising potential of these tools for the understanding of psychiatric diseases, we will present our recent study where we used optogenetic to block abnormal repetitive behavior in a mutant mouse model of obsessive-compulsive disorder [1]. Using a delay-conditioning task we showed that these mutant mouse model had a deficit in response inhibition that lead to repetitive behaviour. With optogenetic, we could stimulate a specific circuitry in the brain that connect the orbitofrontal cortex with the basal ganglia; a circuitry that has been shown to be dysfunctional in compulsive behaviors. We observed that these optogenetic stimulations, through their effect on inhibitory neurons of the basal ganglia, could restore the behavioral response inhibition and alleviate the compulsive behavior. These findings raise promising potential for the design of targeted deep brain stimulation therapy for disorders involving excessive repetitive behavior and/or for the optimization of already existing stimulation protocol [2].

The effect of striatal pre-enkephalin overexpression in the basal ganglia of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease

2014 ◽  
Vol 40 (2) ◽  
pp. 2406-2416 ◽  
Author(s):  
Stéphanie Bissonnette ◽  
Sophie Muratot ◽  
Nathalie Vernoux ◽  
François Bezeau ◽  
Frédéric Calon ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Mouse Model

scholarly journals Adaptative Up-Regulation of PRX2 and PRX5 Expression Characterizes Brain from a Mouse Model of Chorea-Acanthocytosis

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 76
Author(s):  
Enrica Federti ◽  
Alessandro Matte ◽  
Veronica Riccardi ◽  
Kevin Peikert ◽  
Seth L. Alper ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Mouse Model ◽  
Neurodegenerative Disorders ◽  
Crucial Role ◽  
Neuronal Damage ◽  
Mouse Strains ◽  
Wild Type ◽  
Nrf2 Activation ◽  
Regulated Expression ◽  
Age Dependent

The peroxiredoxins (PRXs) constitute a ubiquitous antioxidant. Growing evidence in neurodegenerative disorders such as Parkinson’s disease (PD) or Alzheimer’s disease (AD) has highlighted a crucial role for PRXs against neuro-oxidation. Chorea-acanthocytosis/Vps13A disease (ChAc) is a devastating, life-shortening disorder characterized by acanthocytosis, neurodegeneration and abnormal proteostasis. We recently developed a Vps13a−/− ChAc-mouse model, showing acanthocytosis, neurodegeneration and neuroinflammation which could be restored by LYN inactivation. Here, we show in our Vps13a−/− mice protein oxidation, NRF2 activation and upregulation of downstream cytoprotective systems NQO1, SRXN1 and TRXR in basal ganglia. This was associated with upregulation of PRX2/5 expression compared to wild-type mice. PRX2 expression was age-dependent in both mouse strains, whereas only Vps13a−/− PRX5 expression was increased independent of age. LYN deficiency or nilotinib-mediated LYN inhibition improved autophagy in Vps13a−/− mice. In Vps13a−/−; Lyn−/− basal ganglia, absence of LYN resulted in reduced NRF2 activation and down-regulated expression of PRX2/5, SRXN1 and TRXR. Nilotinib treatment of Vps13a−/− mice reduced basal ganglia oxidation, and plasma PRX5 levels, suggesting plasma PRX5 as a possible ChAc biomarker. Our data support initiation of therapeutic Lyn inhibition as promptly as possible after ChAc diagnosis to minimize development of irreversible neuronal damage during otherwise inevitable ChAc progression.

Differential consequences of habitual responding in a mouse model of repetitive behavior.

2020 ◽  
Vol 134 (1) ◽  
pp. 21-33 ◽  
Author(s):  
Lisa S. Curry-Pochy ◽  
Zachary Kravetz ◽  
Jessica Feinstein ◽  
Brianna Yaffe ◽  
Vivian Tanios ◽  
...  
Keyword(s):  
Mouse Model ◽  
Repetitive Behavior ◽  
Habitual Responding
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