Characterizing Social Behavior in Genetically Targeted Mouse Models of Brain Disorders

2013 ◽  
pp. 95-104 ◽  
Author(s):  
Emma L. Burrows ◽  
Anthony J. Hannan
Keyword(s):  
Social Behavior ◽  
Mouse Models ◽  
Brain Disorders

scholarly journals Intranasal oxytocin administration ameliorates social behavioral deficits in a POGZWT/Q1038R mouse model of autism spectrum disorder

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Kohei Kitagawa ◽  
Kensuke Matsumura ◽  
Masayuki Baba ◽  
Momoka Kondo ◽  
Tomoya Takemoto ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Social Behavior ◽  
Mouse Model ◽  
Mouse Models ◽  
De Novo ◽  
Neurodevelopmental Disorder ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
De Novo Mutation ◽  
Behavioral Deficits

AbstractAutism spectrum disorder (ASD) is a highly prevalent neurodevelopmental disorder characterized by core symptoms of impaired social behavior and communication. Recent studies have suggested that the oxytocin system, which regulates social behavior in mammals, is potentially involved in ASD. Mouse models of ASD provide a useful system for understanding the associations between an impaired oxytocin system and social behavior deficits. However, limited studies have shown the involvement of the oxytocin system in the behavioral phenotypes in mouse models of ASD. We have previously demonstrated that a mouse model that carries the ASD patient-derived de novo mutation in the pogo transposable element derived with zinc finger domain (POGZWT/Q1038R mice), showed ASD-like social behavioral deficits. Here, we have explored whether oxytocin (OXT) administration improves impaired social behavior in POGZWT/Q1038R mice and found that intranasal oxytocin administration effectively restored the impaired social behavior in POGZWT/Q1038R mice. We also found that the expression level of the oxytocin receptor gene (OXTR) was low in POGZWT/Q1038R mice. However, we did not detect significant changes in the number of OXT-expressing neurons between the paraventricular nucleus of POGZWT/Q1038R mice and that of WT mice. A chromatin immunoprecipitation assay revealed that POGZ binds to the promoter region of OXTR and is involved in the transcriptional regulation of OXTR. In summary, our study demonstrate that the pathogenic mutation in the POGZ, a high-confidence ASD gene, impairs the oxytocin system and social behavior in mice, providing insights into the development of oxytocin-based therapeutics for ASD.

scholarly journals Prioritizing the development of mouse models for childhood brain disorders

2016 ◽  
Vol 100 ◽  
pp. 2-16 ◽  
Author(s):  
Kevin K. Ogden ◽  
Emin D. Ozkan ◽  
Gavin Rumbaugh
Keyword(s):  
Mouse Models ◽  
Brain Disorders

Single administration of resveratrol improves social behavior in adult mouse models of autism spectrum disorder

2020 ◽  
Vol 84 (11) ◽  
pp. 2207-2214 ◽  
Author(s):  
Shizu Hidema ◽  
Shohei Kikuchi ◽  
Ryoji Takata ◽  
Takaaki Yanai ◽  
Kenju Shimomura ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Social Behavior ◽  
Mouse Models ◽  
Adult Mouse ◽  
Autism Spectrum ◽  
Spectrum Disorder ◽  
Single Administration

scholarly journals Genetic underpinnings of sociability in the general population

2021 ◽  
Author(s):  
Janita Bralten ◽  
Nina R. Mota ◽  
Cornelius J. H. M. Klemann ◽  
Ward De Witte ◽  
Emma Laing ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Autism Spectrum Disorders ◽  
Social Behavior ◽  
General Population ◽  
Autism Spectrum ◽  
Polygenic Risk Score ◽  
Brain Disorders ◽  
Polygenic Risk ◽  
Behavior Outcomes ◽  
Spectrum Disorders

AbstractLevels of sociability are continuously distributed in the general population, and decreased sociability represents an early manifestation of several brain disorders. Here, we investigated the genetic underpinnings of sociability in the population. We performed a genome-wide association study (GWAS) of a sociability score based on four social functioning-related self-report questions from 342,461 adults in the UK Biobank. Subsequently we performed gene-wide and functional follow-up analyses. Robustness analyses were performed in the form of GWAS split-half validation analyses, as well as analyses excluding neuropsychiatric cases. Using genetic correlation analyses as well as polygenic risk score analyses we investigated genetic links of our sociability score to brain disorders and social behavior outcomes. Individuals with autism spectrum disorders, bipolar disorder, depression, and schizophrenia had a lower sociability score. The score was significantly heritable (SNP h2 of 6%). We identified 18 independent loci and 56 gene-wide significant genes, including genes like ARNTL, DRD2, and ELAVL2. Many associated variants are thought to have deleterious effects on gene products and our results were robust. The sociability score showed negative genetic correlations with autism spectrum, disorders, depression, schizophrenia, and two sociability-related traits—loneliness and social anxiety—but not with bipolar disorder or Alzheimer’s disease. Polygenic risk scores of our sociability GWAS were associated with social behavior outcomes within individuals with bipolar disorder and with major depressive disorder. Variation in population sociability scores has a genetic component, which is relevant to several psychiatric disorders. Our findings provide clues towards biological pathways underlying sociability.

scholarly journals GSK-3β at the Intersection of Neuronal Plasticity and Neurodegeneration

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Tomasz Jaworski ◽  
Ewa Banach-Kasper ◽  
Katarzyna Gralec
Keyword(s):  
Synaptic Plasticity ◽  
Mouse Models ◽  
Glycogen Synthase ◽  
Glycogen Synthase Kinase 3 ◽  
Normal Brain ◽  
Brain Disorders ◽  
Pharmacological Interventions ◽  
Brain Functioning ◽  
Behavioral Abnormalities ◽  
Gsk 3Β

In neurons, Glycogen Synthase Kinase-3β (GSK-3β) has been shown to regulate various critical processes underlying structural and functional synaptic plasticity. Mouse models with neuron-selective expression or deletion of GSK-3β present behavioral and cognitive abnormalities, positioning this protein kinase as a key signaling molecule in normal brain functioning. Furthermore, mouse models with defective GSK-3β activity display distinct structural and behavioral abnormalities, which model some aspects of different neurological and neuropsychiatric disorders. Equalizing GSK-3β activity in these mouse models by genetic or pharmacological interventions is able to rescue some of these abnormalities. Thus, GSK-3β is a relevant therapeutic target for the treatment of many brain disorders. Here, we provide an overview of how GSK-3β is regulated in physiological synaptic plasticity and how aberrant GSK-3β activity contributes to the development of dysfunctional synaptic plasticity in neuropsychiatric and neurodegenerative disorders.

scholarly journals Mechanisms Underlying Microbial-Mediated Changes in Social Behavior in Mouse Models of Autism Spectrum Disorder

Neuron ◽  
2019 ◽  
Vol 101 (2) ◽  
pp. 246-259.e6 ◽  
Author(s):  
Martina Sgritta ◽  
Sean W. Dooling ◽  
Shelly A. Buffington ◽  
Eric N. Momin ◽  
Michael B. Francis ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Social Behavior ◽  
Mouse Models ◽  
Autism Spectrum ◽  
Spectrum Disorder

Altered behavior and neural activity in conspecific cagemates co-housed with mouse models of brain disorders

2016 ◽  
Vol 163 ◽  
pp. 167-176 ◽  
Author(s):  
Hyunwoo Yang ◽  
Seungmoon Jung ◽  
Jinsoo Seo ◽  
Arshi Khalid ◽  
Jung-Seok Yoo ◽  
...  
Keyword(s):  
Mouse Models ◽  
Neural Activity ◽  
Brain Disorders
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