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Article: Tspyl2 Loss-of-Function Causes Neurodevelopmental Brain and Behavior Abnormalities in Mice
Title | Tspyl2 Loss-of-Function Causes Neurodevelopmental Brain and Behavior Abnormalities in Mice |
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Authors | |
Keywords | Lateral ventricles Locomotion MRI Prepulse inhibition Tspyl2 |
Issue Date | 2016 |
Publisher | Springer 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? |
Abstract | Testis 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 Identifier | http://hdl.handle.net/10722/231898 |
ISSN | 2023 Impact Factor: 2.6 2023 SCImago Journal Rankings: 1.092 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Li, Q | - |
dc.contributor.author | Chan, SY | - |
dc.contributor.author | Wong, KK | - |
dc.contributor.author | Wei, R | - |
dc.contributor.author | Leung, YO | - |
dc.contributor.author | Ding, AY | - |
dc.contributor.author | Hui, TCK | - |
dc.contributor.author | Cheung, C | - |
dc.contributor.author | Chua, SE | - |
dc.contributor.author | Sham, PC | - |
dc.contributor.author | Wu, EX | - |
dc.contributor.author | McAlonan, GM | - |
dc.date.accessioned | 2016-09-20T05:26:12Z | - |
dc.date.available | 2016-09-20T05:26:12Z | - |
dc.date.issued | 2016 | - |
dc.identifier.citation | Behavior Genetics, 2016, v. 46 n. 4, p. 529-537 | - |
dc.identifier.issn | 0001-8244 | - |
dc.identifier.uri | http://hdl.handle.net/10722/231898 | - |
dc.description.abstract | Testis 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.language | eng | - |
dc.publisher | Springer New York LLC. The Journal's web site is located at http://springerlink.metapress.com/openurl.asp?genre=journal&issn=0001-8244 | - |
dc.relation.ispartof | Behavior Genetics | - |
dc.rights | The final publication is available at Springer via http://dx.doi.org/[insert DOI] | - |
dc.subject | Lateral ventricles | - |
dc.subject | Locomotion | - |
dc.subject | MRI | - |
dc.subject | Prepulse inhibition | - |
dc.subject | Tspyl2 | - |
dc.title | Tspyl2 Loss-of-Function Causes Neurodevelopmental Brain and Behavior Abnormalities in Mice | - |
dc.type | Article | - |
dc.identifier.email | Li, Q: liqi@hkucc.hku.hk | - |
dc.identifier.email | Chan, SY: sychan@hkucc.hku.hk | - |
dc.identifier.email | Hui, TCK: ckhui@hku.hk | - |
dc.identifier.email | Cheung, C: charlton@hkucc.hku.hk | - |
dc.identifier.email | Chua, SE: sechua@hkucc.hku.hk | - |
dc.identifier.email | Sham, PC: pcsham@hku.hk | - |
dc.identifier.email | Wu, EX: ewu@eee.hku.hk | - |
dc.identifier.email | McAlonan, GM: mcalonan@hkucc.hku.hk | - |
dc.identifier.authority | Chan, SY=rp00356 | - |
dc.identifier.authority | Cheung, C=rp01574 | - |
dc.identifier.authority | Chua, SE=rp00438 | - |
dc.identifier.authority | Sham, PC=rp00459 | - |
dc.identifier.authority | Wu, EX=rp00193 | - |
dc.identifier.authority | McAlonan, GM=rp00475 | - |
dc.identifier.doi | 10.1007/s10519-015-9777-8 | - |
dc.identifier.pmcid | PMC4886156 | - |
dc.identifier.scopus | eid_2-s2.0-84955574710 | - |
dc.identifier.hkuros | 263307 | - |
dc.identifier.volume | 46 | - |
dc.identifier.issue | 4 | - |
dc.identifier.spage | 529 | - |
dc.identifier.epage | 537 | - |
dc.identifier.isi | WOS:000376889900005 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0001-8244 | - |