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

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].

scholarly journals Corticostriatal dynamics underlying components of binge-like eating in mice

2021 ◽  
Author(s):  
Britny A Hildebrandt ◽  
Hayley Fisher ◽  
Zoe LaPalombara ◽  
Michael E Young ◽  
Susanne E Ahmari
Keyword(s):  
Neural Activity ◽  
Negative Impact ◽  
Repetitive Behavior ◽  
Clinical Work ◽  
Palatable Food ◽  
Clinical Model ◽  
Compulsive Disorder ◽  
Increased Risk ◽  
Habitual Responding

Binge eating (BE) is a maladaptive repetitive feeding behavior present across nearly all eating disorder diagnoses. BE is associated with poor psychosocial outcomes (e.g., suicidal ideation) and increased risk for obesity. Despite the substantial negative impact of BE, its underlying neural mechanisms are largely unknown. Many other repetitive behavior disorders (e.g., obsessive compulsive disorder) show dysfunction within corticostriatal circuitry. Additionally, previous pre clinical and clinical work has highlighted an imbalance between goal directed and habitual responding in BE. The aim of the current study was to longitudinally examine in vivo neural activity within corticostriatal regions associated with habitual behavior, the infralimbic cortex (IL) and dorsolateral striatum (DLS), using a robust pre clinical model for BE. Female C57BL/6 mice (N = 32) were randomized to receive: 1) intermittent (daily, 2-hour) binge-like access to palatable food (BE mice), or 2) continuous, non-intermittent (24-hour) access to palatable food (non-BE mice). In vivo calcium imaging was performed via fiber photometry at the baseline timepoint and after 4 weeks (chronic timepoint) of engagement in the model for BE. Feeding behaviors (feeding bout onset, offset) during the recordings were captured using contact lickometers which generated TTL outputs for precise alignment of BE behavior to neural data. Results in the IL showed no specific changes in neural activity related to BE. However, BE animals showed decreased DLS activity from the baseline to chronic timepoint at feeding onset and offset. Additionally, BE mice had significantly lower DLS activity at feeding onset and offset during the chronic time point compared to non-BE mice. These results point to a role for DLS hypofunction in chronic BE, highlighting a potential target for future treatment intervention.

scholarly journals Vorinostat corrects cognitive and non-cognitive symptoms in a mouse model of fragile X syndrome

2020 ◽  
Author(s):  
Qi Ding ◽  
Xueting Wu ◽  
Xuan Li ◽  
Hongbing Wang
Keyword(s):  
Mouse Model ◽  
Fragile X Syndrome ◽  
Fragile X ◽  
Repetitive Behavior ◽  
Clinical Intervention ◽  
Behavioral Symptoms ◽  
Therapeutic Effects ◽  
Object Location Memory ◽  
Approved Drugs ◽  
Cellular Pathology

ABSTRACTFragile X syndrome (FXS) is caused by mutations in the FMR1 (fragile X mental retardation 1) gene. It is a significant form of heritable intellectual disability with comorbidity of other symptoms such as autism. Due to the lack of efficacious medication, repurposing the existing FDA-approved drugs may offer an opportunity to advance clinical intervention for FXS. Analysis of the whole-genome transcription signatures predicts new therapeutic action of vorinostat to correct pathological alterations associated with FXS. We further find that the administration of vorinostat restores object location memory and passive avoidance memory in the Fmr1 knockout (KO) mice. For the non-cognitive behavioral symptoms, vorinostat corrects the autism-associated alterations, including repetitive behavior and social interaction deficits. In the open field test, vorinostat dampens hyperactivity in the center area of the arena. Surprisingly, vorinostat does not affect the abnormally elevated protein synthesis in Fmr1 KO neurons, suggesting different outcomes from correcting behavioral symptoms and specific aspects of cellular pathology. Our data reveal the therapeutic effects of the FDA-approved drug vorinostat in a mouse model of FXS and advocate efficacy testing with human patients.

scholarly journals Serotonin 6 receptor blockade reduces repetitive behavior in the BTBR mouse model of autism spectrum disorder

2021 ◽  
Vol 200 ◽  
pp. 173076
Author(s):  
Dionisio A. Amodeo ◽  
Brandon Oliver ◽  
Alma Pahua ◽  
Kristianna Hitchcock ◽  
Alexa Bykowski ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Mouse Model ◽  
Repetitive Behavior ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Receptor Blockade ◽  
Btbr Mouse

Human adipose-derived stem cells ameliorate repetitive behavior, social deficit and anxiety in a VPA-induced autism mouse model

2017 ◽  
Vol 317 ◽  
pp. 479-484 ◽  
Author(s):  
Sungji Ha ◽  
Hyunjun Park ◽  
Usman Mahmood ◽  
Jeong Chan Ra ◽  
Yoo-Hun Suh ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mouse Model ◽  
Repetitive Behavior ◽  
Adipose Derived Stem Cells ◽  
Social Deficit

scholarly journals Repetitive behavior profile and supersensitivity to amphetamine in the C58/J mouse model of autism

2014 ◽  
Vol 259 ◽  
pp. 200-214 ◽  
Author(s):  
Sheryl S. Moy ◽  
Natallia V. Riddick ◽  
Viktoriya D. Nikolova ◽  
Brian L. Teng ◽  
Kara L. Agster ◽  
...  
Keyword(s):  
Mouse Model ◽  
Repetitive Behavior ◽  
Behavior Profile

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
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