View Item 

Show simple item record

Rodent models of genetic and chromosomal variations in psychiatric disorders
dc.contributor.authorNomura, Jun
dc.contributor.authorKannan, Geetha
dc.contributor.authorTakumi, Toru
dc.date.accessioned2017-10-05T18:19:56Z
dc.date.available2018-11-01T16:42:01Zen
dc.date.issued2017-08
dc.identifier.citationNomura, Jun; Kannan, Geetha; Takumi, Toru (2017). "Rodent models of genetic and chromosomal variations in psychiatric disorders." Psychiatry and Clinical Neurosciences 71(8): 508-517.
dc.identifier.issn1323-1316
dc.identifier.issn1440-1819
dc.identifier.urihttps://hdl.handle.net/2027.42/138393
dc.publisherJohn Wiley & Sons Australia, Ltd
dc.subject.otherearly intervention
dc.subject.otherexcitatory inhibitory balance
dc.subject.othercopy number variation
dc.subject.otherautism
dc.subject.otheranimal models
dc.titleRodent models of genetic and chromosomal variations in psychiatric disorders
dc.typeArticleen_US
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelPsychiatry
dc.subject.hlbsecondlevelNeurosciences
dc.subject.hlbtoplevelHealth Sciences
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttps://deepblue.lib.umich.edu/bitstream/2027.42/138393/1/pcn12524.pdf
dc.description.bitstreamurlhttps://deepblue.lib.umich.edu/bitstream/2027.42/138393/2/pcn12524_am.pdf
dc.identifier.doi10.1111/pcn.12524
dc.identifier.sourcePsychiatry and Clinical Neurosciences
dc.identifier.citedreferencePoot M. Connecting the CNTNAP2 networks with neurodevelopmental disorders. Mol. Syndromol. 2015; 6: 7 – 22.
dc.identifier.citedreferencePeñagarikano O, Abrahams BS, Herman EI et al. Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities, and core autism‐related deficits. Cell 2011; 147: 235 – 246.
dc.identifier.citedreferenceYamasue H. Promising evidence and remaining issues regarding the clinical application of oxytocin in autism spectrum disorders. Psychiatry Clin. Neurosci. 2016; 70: 89 – 99.
dc.identifier.citedreferenceFeifel D, Shilling PD, MacDonald K. A review of oxytocin’s effects on the positive, negative, and cognitive domains of schizophrenia. Biol. Psychiatry 2016; 79: 222 – 233.
dc.identifier.citedreferenceSandi C, Haller J. Stress and the social brain: Behavioural effects and neurobiological mechanisms. Nat. Rev. Neurosci. 2015; 16: 290 – 304.
dc.identifier.citedreferenceVolk L, Chiu S‐L, Sharma K, Huganir RL. Glutamate synapses in human cognitive disorders. Annu. Rev. Neurosci. 2015; 38: 127 – 149.
dc.identifier.citedreferenceHikida T, Mustafa AK, Maeda K et al. Modulation of d‐serine levels in brains of mice lacking PICK1. Biol. Psychiatry 2008; 63: 997 – 1000.
dc.identifier.citedreferenceVolk L, Kim C‐H, Takamiya K, Yu Y, Huganir RL. Developmental regulation of protein interacting with C kinase 1 (PICK1) function in hippocampal synaptic plasticity and learning. Proc. Natl. Acad. Sci. U. S. A. 2010; 107: 21784 – 21789.
dc.identifier.citedreferenceNakamura T, Lipton SA. Protein S‐Nitrosylation as a therapeutic target for neurodegenerative diseases. Trends Pharmacol. Sci. 2015; 37: 73 – 84.
dc.identifier.citedreferenceLandek‐Salgado MA, Faust TE, Sawa A. Molecular substrates of schizophrenia: Homeostatic signaling to connectivity. Mol. Psychiatry 2016; 21: 10 – 28.
dc.identifier.citedreferenceO’Donnell P. Cortical disinhibition in the neonatal ventral hippocampal lesion model of schizophrenia: New vistas on possible therapeutic approaches. Pharmacol. Ther. 2012; 133: 19 – 25.
dc.identifier.citedreferenceVelasco I, Salazar P, Giorgetti A et al. Concise review: Generation of neurons from somatic cells of healthy individuals and neurological patients through induced pluripotency or direct conversion. Stem Cells 2014; 32: 2811 – 2817.
dc.identifier.citedreferenceNageshappa S, Carromeu C, Trujillo CA, Mesci P, Pasciuto E, Vanderhaeghen P. Altered neuronal network and rescue in a human MECP2 duplication model. Mol. Psychiatry 2016; 21: 178 – 188.
dc.identifier.citedreferenceSupekar K, Uddin LQ, Khouzam A et al. Brain hyperconnectivity in children with autism and its links to social deficits. Cell Rep. 2013; 5: 738 – 747.
dc.identifier.citedreferenceDi Martino A, Yan C‐G, Li Q et al. The autism brain imaging data exchange: Towards a large‐scale evaluation of the intrinsic brain architecture in autism. Mol. Psychiatry 2014; 19: 659 – 667.
dc.identifier.citedreferenceVadodaria KC, Mertens J, Paquola A et al. Generation of functional human serotonergic neurons from fibroblasts. Mol. Psychiatry 2016; 21: 49 – 61.
dc.identifier.citedreferenceSmeets EEJ, Pelc K, Dan B. Rett syndrome. Mol. Syndromol. 2011; 2: 113 – 127.
dc.identifier.citedreferenceMullard A. Fragile X disappointments upset autism ambitions. Nat. Rev. Drug Discov. 2015; 14: 151 – 153.
dc.identifier.citedreferenceMullard A. Fragile X drug development flounders. Nat. Rev. Drug Discov. 2016; 15: 77.
dc.identifier.citedreferenceHao S, Tang B, Wu Z et al. Forniceal deep brain stimulation rescues hippocampal memory in Rett syndrome mice. Nature 2015; 526: 430 – 434.
dc.identifier.citedreferenceFerenczi E, Deisseroth K. Illuminating next‐generation brain therapies. Nat. Neurosci. 2016; 19: 414 – 416.
dc.identifier.citedreferenceAkbarian S, Sucher NJ, Bradley D et al. Selective alterations in gene expression for NMDA receptor subunits in prefrontal cortex of schizophrenics. J. Neurosci. 1996; 16: 19 – 30.
dc.identifier.citedreferenceColantuoni C, Jeon OH, Hyder K et al. Gene expression profiling in postmortem Rett syndrome brain: Differential gene expression and patient classification. Neurobiol. Dis. 2001; 8: 847 – 865.
dc.identifier.citedreferenceSebat J, Lakshmi B, Troge J, Alexander J, Young J. Large‐scale copy number polymorphism in the human genome. Science 2004; 305: 525 – 528.
dc.identifier.citedreferenceEichler SA, Meier JC. E‐I balance and human diseases: From molecules to networking. Front. Mol. Neurosci. 2008; 1: 2.
dc.identifier.citedreferenceNelson SB, Valakh V. Review excitatory/inhibitory balance and circuit homeostasis in autism spectrum disorders. Neuron 2015; 87: 684 – 698.
dc.identifier.citedreferenceArgyropoulos A, Gilby KL, Hill‐Yardin EL. Studying autism in rodent models: Reconciling endophenotypes with comorbidities. Front. Hum. Neurosci. 2013; 7: 1 – 10.
dc.identifier.citedreferenceStafstrom CE. Epilepsy: A review of selected clinical syndromes and advances in basic science. J. Cereb. Blood Flow Metab. 2006; 26: 983 – 1004.
dc.identifier.citedreferenceMariani J, Coppola G, Zhang P et al. FOXG1‐dependent dysregulation of GABA/glutamate neuron differentiation in autism spectrum disorders. Cell 2015; 162: 375 – 390.
dc.identifier.citedreferencePocklington AJ, Rees E, Walters JTR et al. Novel findings from CNVs implicate inhibitory and excitatory signaling complexes in schizophrenia. Neuron 2015; 86: 1203 – 1214.
dc.identifier.citedreferenceBlue ME, Naidu S, Johnston MV. Altered development of glutamate and GABA receptors in the basal ganglia of girls with Rett syndrome. Exp. Neurol. 1999; 156: 345 – 352.
dc.identifier.citedreferenceYizhar O, Fenno LE, Prigge M et al. Neocortical excitation/inhibition balance in information processing and social dysfunction. Nature 2011; 477: 171 – 178.
dc.identifier.citedreferenceBrown JA, Ramikie TS, Schmidt MJ et al. Inhibition of parvalbumin‐expressing interneurons results in complex behavioral changes. Mol. Psychiatry 2015; 20: 1499 – 1507.
dc.identifier.citedreferenceBarnes S, Pinto‐Duarte A, Kappe A et al. Disruption of mGluR5 in parvalbumin‐positive interneurons induces core features of neurodevelopmental disorders. Mol. Psychiatry 2015; 20: 1161 – 1172.
dc.identifier.citedreferenceChung W, Choi SY, Lee E et al. Social deficits in IRSp53 mutant mice improved by NMDAR and mGluR5 suppression. Nat. Neurosci. 2015; 18: 435 – 443.
dc.identifier.citedreferenceLee K‐W, Westin L, Kim J et al. Alteration by p11 of mGluR5 localization regulates depression‐like behaviors. Mol. Psychiatry 2015; 20: 1546 – 1556.
dc.identifier.citedreferenceLyst MJ, Bird A. Rett syndrome: A complex disorder with simple roots. Nat. Rev. Genet. 2015; 16: 261 – 275.
dc.identifier.citedreferencePatrizi A, Picard N, Simon AJ et al. Chronic administration of the N‐methyl‐D‐aspartate receptor antagonist ketamine improves Rett syndrome phenotype. Biol. Psychiatry 2016; 79: 755 – 764.
dc.identifier.citedreferenceBurette AC, Park H, Weinberg RJ. Postsynaptic distribution of IRSp53 in spiny excitatory and inhibitory neurons. J. Comp. Neurol. 2014; 522: 2164 – 2178.
dc.identifier.citedreferenceThankachan S, Mckenna JT, Mcnally JM et al. Correction for Kim et al., cortically projecting basal forebrain parvalbumin neurons regulate cortical gamma band oscillations. Proc. Natl. Acad. Sci. U. S. A. 2015; 112: 3535 – 3540.
dc.identifier.citedreferenceMalhotra D, Sebat J. CNVs: Harbingers of a rare variant revolution in psychiatric genetics. Cell 2012; 148: 1223 – 1241.
dc.identifier.citedreferenceLi HH, Roy M, Kuscuoglu U et al. Induced chromosome deletions cause hypersociability and other features of Williams‐Beuren syndrome in mice. EMBO Mol. Med. 2009; 1: 50 – 65.
dc.identifier.citedreferenceNakatani J, Tamada K, Hatanaka F et al. Abnormal behavior in a chromosome‐ engineered mouse model for human 15q11‐13 duplication seen in autism. Cell 2009; 137: 1235 – 1246.
dc.identifier.citedreferenceFejgin K, Nielsen J, Birknow MR et al. A mouse model that recapitulates cardinal features of the 15q13.3 microdeletion syndrome including schizophrenia‐ and epilepsy‐related alterations. Biol. Psychiatry 2014; 76: 128 – 137.
dc.identifier.citedreferenceKogan JH, Gross AK, Featherstone RE et al. Mouse model of chromosome 15q13.3 microdeletion syndrome demonstrates features related to autism spectrum disorder. J. Neurosci. 2015; 35: 16282 – 16294.
dc.identifier.citedreferenceHorev G, Ellegood J, Lerch JP et al. Dosage‐dependent phenotypes in models of 16p11.2 lesions found in autism. Proc. Natl. Acad. Sci. U. S. A. 2011; 108: 17076 – 17081.
dc.identifier.citedreferenceWalz K, Caratini‐Rivera S, Bi W et al. Modeling del(17)(p11.2p11.2) and dup(17)(p11.2p11.2) contiguous gene syndromes by chromosome engineering in mice: Phenotypic consequences of gene dosage imbalance. Mol. Cell. Biol. 2003; 23: 3646 – 3655.
dc.identifier.citedreferenceStark KL, Xu B, Bagchi A et al. Altered brain microRNA biogenesis contributes to phenotypic deficits in a 22q11‐deletion mouse model. Nat. Genet. 2008; 40: 751 – 760.
dc.identifier.citedreferenceNomura J, Takumi T. Animal models of psychiatric disorders that reflect human copy number variation. Neural Plast. 2012; 2012: 589524.
dc.identifier.citedreferenceCook EH, Scherer SW. Copy‐number variations associated with neuropsychiatric conditions. Nature 2008; 455: 919 – 923.
dc.identifier.citedreferenceTamada K, Tomonaga S, Hatanaka F et al. Decreased exploratory activity in a mouse model of 15q duplication syndrome; Implications for disturbance of serotonin signaling. PLoS ONE 2010; 5: e15126.
dc.identifier.citedreferenceKishimoto R, Tamada K, Liu X et al. Model mice for 15q11–13 duplication syndrome exhibit late‐onset obesity and altered lipid metabolism. Hum. Mol. Genet. 2015; 24: 4559 – 4572.
dc.identifier.citedreferenceMarini C, Cecconi A, Contini E et al. Clinical and genetic study of a family with a paternally inherited 15q11‐q13 duplication. Am. J. Med. Genet. Part A 2013; 161: 1459 – 1464.
dc.identifier.citedreferenceWang SSH, Kloth AD, Badura A. The cerebellum, sensitive periods, and autism. Neuron 2014; 83: 518 – 532.
dc.identifier.citedreferencePiochon C, Kloth AD, Grasselli G et al. Cerebellar plasticity and motor learning deficits in a copy‐number variation mouse model of autism. Nat. Commun. 2014; 5: 5586.
dc.identifier.citedreferenceKloth AD, Badura A, Li A et al. Cerebellar associative sensory learning defects in five mouse autism models. Elife 2015; 4: 1 – 26.
dc.identifier.citedreferenceEllegood J, Anagnostou E, Babineau BA et al. Clustering autism: Using neuroanatomical differences in 26 mouse models to gain insight into the heterogeneity. Mol. Psychiatry 2015; 20: 118 – 125.
dc.identifier.citedreferenceEllegood J, Anagnostou E, Babineau BA et al. 3D visualization of the regional differences. Mol. Psychiatry 2015; 20: 1.
dc.identifier.citedreferenceEllegood J, Nakai N, Nakatani J, Henkelman M, Takumi T, Lerch J. Neuroanatomical phenotypes are consistent with autism‐like behavioral phenotypes in the 15q11‐13 duplication mouse model. Autism Res. 2015; 8: 545 – 555.
dc.identifier.citedreferenceIto M, Yamaguchi K, Nagao S, Yamazaki T. Long‐term depression as a model of cerebellar plasticity. Prog. Brain Res. 2014; 210: 1 – 30.
dc.identifier.citedreferenceBurnside RD. 22q11.21 deletion syndromes: A review of proximal, central, and distal deletions and their associated features. Cytogenet. Genome Res. 2015; 146: 89 – 99.
dc.identifier.citedreferenceMichaelovsky E, Frisch A, Carmel M et al. Genotype‐phenotype correlation in 22q11.2 deletion syndrome. BMC Med. Genet. 2012; 13: 1 – 11.
dc.identifier.citedreferenceSchneider M, Debbané M, Bassett AS et al. Psychiatric disorders from childhood to adulthood in 22q11.2 deletion syndrome: Results from the International Consortium on Brain and Behavior in 22q11.2 Deletion Syndrome. Am. J. Psychiatry 2014; 171: 627 – 639.
dc.identifier.citedreferenceJerome L, Papaioannou V. DiGeorge syndrome phenotype in mice mutant for the T‐box gene, Tbx1. Nat. Genet. 2001; 27: 286 – 291.
dc.identifier.citedreferencePaylor R, Glaser B, Mupod A et al. Tbx1 haploinsufficiency is linked to behavioral disorders in mice and humans: Implications for 22q11 deletion syndrome. Proc. Natl. Acad. Sci. U. S. A. 2006; 103: 7729 – 7734.
dc.identifier.citedreferenceHiramoto T, Kang G, Suzuki G et al. Tbx1: Identification of a 22q11.2 gene as a risk factor for autism spectrum disorder in a mouse model. Hum. Mol. Genet. 2011; 20: 4775 – 4785.
dc.identifier.citedreferenceTakahashi T, Okabe S, Broin P et al. Structure and function of neonatal social communication in a genetic mouse model of autism. Mol. Psychiatry 2016; 21: 1208 – 1214.
dc.identifier.citedreferenceJavitt DC, Freedman R. Sensory processing dysfunction in the personal experience and neuronal machinery of schizophrenia. Am. J. Psychiatry 2015; 172: 17 – 31.
dc.identifier.citedreferenceBurger K, Gullerova M. Swiss army knives: Non‐canonical functions of nuclear Drosha and Dicer. Nat. Rev. Mol. Cell Biol. 2015; 16: 417 – 430.
dc.identifier.citedreferenceXu B, Hsu PK, Stark KL, Karayiorgou M, Gogos JA. Derepression of a neuronal inhibitor due to miRNA dysregulation in a schizophrenia‐related microdeletion. Cell 2013; 152: 262 – 275.
dc.identifier.citedreferenceOuchi Y, Banno Y, Shimizu Y et al. Reduced adult hippocampal neurogenesis and working memory deficits in the Dgcr8‐deficient mouse model of 22q11.2 deletion‐associated schizophrenia can be rescued by IGF2. J. Neurosci. 2013; 33: 9408 – 9419.
dc.identifier.citedreferenceMukai J, Tamura M, Fénelon K et al. Molecular substrates of altered axonal growth and brain connectivity in a mouse model of schizophrenia. Neuron 2015; 86: 680 – 695.
dc.identifier.citedreferenceRamocki MB, Tavyev YJ, Peters SU. The MECP2 duplication syndrome. Am. J. Med. Genet. A 2010; 152A: 1079 – 1088.
dc.identifier.citedreferenceMeins M, Lehmann J, Gerresheim F et al. Submicroscopic duplication in Xq28 causes increased expression of the MECP2 gene in a boy with severe mental retardation and features of Rett syndrome. J. Med. Genet. 2005; 42: e12.
dc.identifier.citedreferenceSztainberg Y, Chen H, Swann JW et al. Reversal of phenotypes in MECP2 duplication mice using genetic rescue or antisense oligos. Nature 2015; 528: 123 – 126.
dc.identifier.citedreferencePeñagarikano O, Lázaro MT, Lu X‐H et al. Exogenous and evoked oxytocin restores social behavior in the Cntnap2 mouse model of autism. Sci. Transl. Med. 2015; 7: 271ra8.
dc.identifier.citedreferenceNomura J, Jaaro‐Peled H, Lewis E et al. Role for neonatal D‐serine signaling: Prevention of physiological and behavioral deficits in adult Pick1 knockout mice. Mol. Psychiatry 2016; 21: 386 – 393.
dc.identifier.citedreferenceCabungcal JH, Counotte DS, Lewis EM et al. Juvenile antioxidant treatment prevents adult deficits in a developmental model of schizophrenia. Neuron 2014; 83: 1073 – 1084.
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Name:
pcn12524.pdf
Size:
123.5KB
Format:
PDF
View/Open
Name:
pcn12524_am.pdf
Size:
476.7KB
Format:
PDF
View/Open

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.