Juvenile manifestation of ultrasound communication deficits in the neuroligin-4 null mutant mouse model of autism

Ju, Anes; Hammerschmidt, Kurt; Tantra, Martesa; Krueger, Dilja D.; Brose, Nils; Ehrenreich, Hannelore

doi:10.1016/j.bbr.2014.05.019

Cited by 54 publications

(35 citation statements)

References 23 publications

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“…Interestingly, pups born to heterozygous Tsc2 +/-females produce fewer USVs after reunion, suggesting deficits in mother-pup interaction (GreeneColozzi et al, 2014;Young et al, 2010). Several ASD animal models show deficits in USVs of pups after maternal separation (Fujita et al, 2008;Shu et al, 2005), as in the case of various mouse models with mutations in Shank1 and Shank3 (Ey et al, 2013;Schmeisser et al, 2012;Wohr, 2014;Wohr et al, 2011;Yang et al, 2012), and in female Nlgn4 -/-mice (Ju et al, 2014). During the reciprocal social interaction task, adult males emit USVs that can be evaluated to assess communication induced by females.…”

Section: Communicationmentioning

confidence: 95%

“…Resident-intruder test Jiang-Xie et al, 2014a;Page, 2014, 2015. Communication Ultrasonic vocalization Pup isolation from mother Wohr et al2011;Schmeisser et al 2012;Yang et al 2012;Ey et al 2013;Wohr 2014,GreeneColozzi et al2014Scattoni et al, 2009;Young et al, 2010;Fujita et al, 2008;Shu et al, 2005;Ju et al, 2014. Female-male/malemale interaction Bozdagi et al 2010;Wohr et al 2011;Schmeisser et al 2012;Won et al 2012; Discrimination of social odors Olfactory discrimination tasks Tsai et al, 2012;Rabaneda et al, 2014. Restricted and repetitive patterns of behavior…”

Section: Aggressionmentioning

confidence: 98%

See 1 more Smart Citation

Autism Spectrum Disorders: Translating human deficits into mouse behavior

Pasciuto

Borrie

Kanellopoulos

et al. 2015

Neurobiology of Learning and Memory

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Section: Communicationmentioning

confidence: 95%

Section: Aggressionmentioning

confidence: 98%

Autism Spectrum Disorders: Translating human deficits into mouse behavior

Pasciuto

Borrie

Kanellopoulos

et al. 2015

Neurobiology of Learning and Memory

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“…Mutants of NLGN4 gene, which encodes for neuroligin-4, a synaptic cell adhesion protein have been shown to display autistic-like behaviors, including social interaction deficits and alterations of ultrasound communication in early developmental stages (Jamain et al, 2008; Ju et al, 2014); to the best of our knowledge, however, no TS-related endophenotypes have been tested in these mutants. Interestingly, NLGN4 KO mice feature decreased excitability in the somatosensory cortical networks (Delattre et al, 2013); further studies are needed to establish whether these functional deficits may be related to the observed thinning of somatosensory cortex in TS patients (Fahim et al, 2010; see Section 3.3).…”

Section: Animal Models Based On Genetic Manipulationsmentioning

confidence: 99%

Animal models of tic disorders: A translational perspective

Godar

Mosher

Giovanni

et al. 2014

Journal of Neuroscience Methods

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Tics are repetitive, sudden movements and/or vocalizations, typically enacted as maladaptive responses to intrusive premonitory urges. The most severe tic disorder, Tourette syndrome (TS), is a childhood-onset condition featuring multiple motor and at least one phonic tic for a duration longer than 1 year. The pharmacological treatment of TS is mainly based on antipsychotic agents; while these drugs are often effective in reducing tic severity and frequency, their therapeutic compliance is limited by serious motor and cognitive side effects. The identification of novel therapeutic targets and development of better treatments for tic disorders is conditional on the development of animal models with high translational validity. In addition, these experimental tools can prove extremely useful to test hypotheses on the etiology and neurobiological bases of TS and related conditions. In recent years, the translational value of these animal models has been enhanced, thanks to a significant re-organization of our conceptual framework of neuropsychiatric disorders, with a greater focus on endophenotypes and quantitative indices, rather than qualitative descriptors. Given the complex and multifactorial nature of TS and other tic disorders, the selection of animal models that can appropriately capture specific symptomatic aspects of these conditions can pose significant theoretical and methodological challenges. In this article, we will review the state of the art on the available animal models of tic disorders, based on genetic mutations, environmental interventions as well as pharmacological manipulations. Furthermore, we will outline emerging lines of translational research showing how some of these experimental preparations have led to significant progress in the identification of novel therapeutic targets for tic disorders.

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“…In both the MIA model of ASD and in BTBR T+ tf/J mice, an increase in the number and duration of vocalization calls compared to controls has been observed (Scattoni et al 2008; Schwartzer et al 2013). In contrast, results of ultrasonic vocalization measurements in reelin heterozygous deficient (RLN+/−) transgenic mice are inconsistent (Romano et al 2013; Michetti et al 2014), while the neuroligin-4 null mutant mouse (another ASD model) presents decreased vocalizations (Ju et al 2014). In recent years, vocalization patterns reflecting a shift of call distribution in different call categories within recorded sonograms are being analyzed, providing better insights on the changes observed in ASD mouse models (Scattoni et al 2008; Silverman et al 2010; Romano et al 2013; Michetti et al 2014).…”

Section: Commentarymentioning

confidence: 99%

Behavioral Phenotyping for Autism Spectrum Disorders in Mice

2017

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Autism spectrum disorder (ASD) represents a heterogeneous group of disorders characterized by alterations in three behavioral symptom domains: social interactions, verbal and nonverbal communication, and repetitive behaviors. Increasing prevalence of ASD in recent years suggests that exposure to environmental toxicants may be critical in modulating etiology of this disease. As clinical diagnosis of autism still relies on behavioral evaluation, it is important to be able to assess similar behavioral traits in animal models, to provide biological plausibility of associations between environmental exposures and ASD. Rodents naturally exhibit a large number of behaviors that can be linked to similar behaviors in human. In this unit, behavioral tests are described that are relevant to the domains affected in ASD. For the repetitive domain, the T-maze spontaneous alternation test and marble burying test are described. For the communication domain, neonatal ultrasonic vocalization and olfactory habituation test toward social and non-social odor are described. Finally, for the sociability domain, the three chambered social preference test and the reciprocal interaction test are presented.

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Juvenile manifestation of ultrasound communication deficits in the neuroligin-4 null mutant mouse model of autism

Cited by 54 publications

References 23 publications

Autism Spectrum Disorders: Translating human deficits into mouse behavior

Autism Spectrum Disorders: Translating human deficits into mouse behavior

Animal models of tic disorders: A translational perspective

Behavioral Phenotyping for Autism Spectrum Disorders in Mice

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