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Article: Tspyl2 Loss-of-Function Causes Neurodevelopmental Brain and Behavior Abnormalities in Mice

TitleTspyl2 Loss-of-Function Causes Neurodevelopmental Brain and Behavior Abnormalities in Mice
Authors
Issue Date2016
PublisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0001-8244
Citation
Behavior Genetics, 2016, v. 46 n. 4, p. 529-537 How to Cite?
AbstractTestis specific protein, Y-encoded-like 2 (TSPYL2) regulates the expression of genes encoding glutamate receptors. Glutamate pathology is implicated in neurodevelopmental conditions such as autism spectrum disorder, attention deficit hyperactivity disorder (ADHD) and schizophrenia. In line with this, a microduplication incorporating the TSPYL2 locus has been reported in people with ADHD. However, the role of Tspyl2 remains unclear. Therefore here we used a Tspyl2 loss-of-function mouse model to directly examine how this gene impacts upon behavior and brain anatomy. We hypothesized that Tspyl2 knockout (KO) would precipitate a phenotype relevant to neurodevelopmental conditions. In line with this prediction, we found that Tspyl2 KO mice were marginally more active, had significantly impaired prepulse inhibition, and were significantly more 'sensitive' to the dopamine agonist amphetamine. In addition, the lateral ventricles were significantly smaller in KO mice. These findings suggest that disrupting Tspyl2 gene expression leads to behavioral and brain morphological alterations that mirror a number of neurodevelopmental psychiatric traits.
Persistent Identifierhttp://hdl.handle.net/10722/231898
ISSN
2015 Impact Factor: 3.268
2015 SCImago Journal Rankings: 1.457
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorLi, Q-
dc.contributor.authorChan, SY-
dc.contributor.authorWong, KK-
dc.contributor.authorWei, R-
dc.contributor.authorLeung, YO-
dc.contributor.authorDing, AY-
dc.contributor.authorHui, TCK-
dc.contributor.authorCheung, C-
dc.contributor.authorChua, SE-
dc.contributor.authorSham, PC-
dc.contributor.authorWu, EX-
dc.contributor.authorMcAlonan, GM-
dc.date.accessioned2016-09-20T05:26:12Z-
dc.date.available2016-09-20T05:26:12Z-
dc.date.issued2016-
dc.identifier.citationBehavior Genetics, 2016, v. 46 n. 4, p. 529-537-
dc.identifier.issn0001-8244-
dc.identifier.urihttp://hdl.handle.net/10722/231898-
dc.description.abstractTestis specific protein, Y-encoded-like 2 (TSPYL2) regulates the expression of genes encoding glutamate receptors. Glutamate pathology is implicated in neurodevelopmental conditions such as autism spectrum disorder, attention deficit hyperactivity disorder (ADHD) and schizophrenia. In line with this, a microduplication incorporating the TSPYL2 locus has been reported in people with ADHD. However, the role of Tspyl2 remains unclear. Therefore here we used a Tspyl2 loss-of-function mouse model to directly examine how this gene impacts upon behavior and brain anatomy. We hypothesized that Tspyl2 knockout (KO) would precipitate a phenotype relevant to neurodevelopmental conditions. In line with this prediction, we found that Tspyl2 KO mice were marginally more active, had significantly impaired prepulse inhibition, and were significantly more 'sensitive' to the dopamine agonist amphetamine. In addition, the lateral ventricles were significantly smaller in KO mice. These findings suggest that disrupting Tspyl2 gene expression leads to behavioral and brain morphological alterations that mirror a number of neurodevelopmental psychiatric traits.-
dc.languageeng-
dc.publisherSpringer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0001-8244-
dc.relation.ispartofBehavior Genetics-
dc.rightsThe final publication is available at Springer via http://dx.doi.org/[insert DOI]-
dc.titleTspyl2 Loss-of-Function Causes Neurodevelopmental Brain and Behavior Abnormalities in Mice-
dc.typeArticle-
dc.identifier.emailLi, Q: liqi@hkucc.hku.hk-
dc.identifier.emailChan, SY: sychan@hkucc.hku.hk-
dc.identifier.emailHui, TCK: ckhui@hku.hk-
dc.identifier.emailCheung, C: charlton@hkucc.hku.hk-
dc.identifier.emailChua, SE: sechua@hkucc.hku.hk-
dc.identifier.emailSham, PC: pcsham@hku.hk-
dc.identifier.emailWu, EX: ewu@eee.hku.hk-
dc.identifier.emailMcAlonan, GM: mcalonan@hkucc.hku.hk-
dc.identifier.authorityChan, SY=rp00356-
dc.identifier.authorityCheung, C=rp01574-
dc.identifier.authorityChua, SE=rp00438-
dc.identifier.authoritySham, PC=rp00459-
dc.identifier.authorityWu, EX=rp00193-
dc.identifier.authorityMcAlonan, GM=rp00475-
dc.identifier.doi10.1007/s10519-015-9777-8-
dc.identifier.pmcidPMC4886156-
dc.identifier.hkuros263307-
dc.identifier.volume46-
dc.identifier.issue4-
dc.identifier.spage529-
dc.identifier.epage537-
dc.publisher.placeUnited States-

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