Reversal of synaptic and behavioral deficits in a 16p11.2 duplication mouse model via restoration of the GABA synapse regulator Npas4
The human 16p11.2 gene locus is a hot spot for copy number variations, which predispose carriers to a range of neuropsychiatric phenotypes. Microduplications of 16p11.2 are associated with autism spectrum disorder (ASD), intellectual disability (ID), and schizophrenia (SZ). Despite the debilitating...
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| Veröffentlicht in: | Molecular psychiatry 2021-06, Vol.26 (6), p.1967-1979 |
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| container_issue | 6 |
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| container_title | Molecular psychiatry |
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| creator | Rein, Benjamin Tan, Tao Yang, Fengwei Wang, Wei Williams, Jamal Zhang, Freddy Mills, Alea Yan, Zhen |
| description | The human 16p11.2 gene locus is a hot spot for copy number variations, which predispose carriers to a range of neuropsychiatric phenotypes. Microduplications of 16p11.2 are associated with autism spectrum disorder (ASD), intellectual disability (ID), and schizophrenia (SZ). Despite the debilitating nature of 16p11.2 duplications, the underlying molecular mechanisms remain poorly understood. Here we performed a comprehensive behavioral characterization of 16p11.2 duplication mice (16p11.2
dp/+
) and identified social and cognitive deficits reminiscent of ASD and ID phenotypes. 16p11.2
dp/+
mice did not exhibit the SZ-related sensorimotor gating deficits, psychostimulant-induced hypersensitivity, or motor impairment. Electrophysiological recordings of 16p11.2
dp/+
mice found deficient GABAergic synaptic transmission and elevated neuronal excitability in the prefrontal cortex (PFC), a brain region critical for social and cognitive functions. RNA-sequencing identified genome-wide transcriptional aberrance in the PFC of 16p11.2
dp/+
mice, including downregulation of the GABA synapse regulator
Npas4
. Restoring
Npas4
expression in PFC of 16p11.2
dp/+
mice ameliorated the social and cognitive deficits and reversed GABAergic synaptic impairment and neuronal hyperexcitability. These findings suggest that prefrontal cortical GABAergic synaptic circuitry and Npas4 are strongly implicated in 16p11.2 duplication pathology, and may represent potential targets for therapeutic intervention in ASD. |
| doi_str_mv | 10.1038/s41380-020-0693-9 |
| format | Article |
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dp/+
) and identified social and cognitive deficits reminiscent of ASD and ID phenotypes. 16p11.2
dp/+
mice did not exhibit the SZ-related sensorimotor gating deficits, psychostimulant-induced hypersensitivity, or motor impairment. Electrophysiological recordings of 16p11.2
dp/+
mice found deficient GABAergic synaptic transmission and elevated neuronal excitability in the prefrontal cortex (PFC), a brain region critical for social and cognitive functions. RNA-sequencing identified genome-wide transcriptional aberrance in the PFC of 16p11.2
dp/+
mice, including downregulation of the GABA synapse regulator
Npas4
. Restoring
Npas4
expression in PFC of 16p11.2
dp/+
mice ameliorated the social and cognitive deficits and reversed GABAergic synaptic impairment and neuronal hyperexcitability. These findings suggest that prefrontal cortical GABAergic synaptic circuitry and Npas4 are strongly implicated in 16p11.2 duplication pathology, and may represent potential targets for therapeutic intervention in ASD.</description><identifier>ISSN: 1359-4184</identifier><identifier>EISSN: 1476-5578</identifier><identifier>DOI: 10.1038/s41380-020-0693-9</identifier><identifier>PMID: 32099100</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/89 ; 38/39 ; 38/77 ; 45/91 ; 631/378 ; 692/699/476/1373 ; 9/74 ; Autism ; Behavioral Sciences ; Biological Psychology ; Care and treatment ; Chromosome 16 ; Cognitive ability ; Copy number ; Copy number variations ; Development and progression ; Excitability ; GABA ; Genetic aspects ; Genomes ; Health aspects ; Hypersensitivity ; Intellectual disabilities ; Medicine ; Medicine & Public Health ; Mental disorders ; Molecular modelling ; Mutation hot spots ; Neurosciences ; Neurotransmitters ; Pervasive developmental disorders ; Pharmacotherapy ; Phenotypes ; Physiological aspects ; Prefrontal cortex ; Psychiatry ; Schizophrenia ; Sensorimotor gating ; Synapses ; Synaptic transmission ; Transcription ; Transcription factors ; γ-Aminobutyric acid</subject><ispartof>Molecular psychiatry, 2021-06, Vol.26 (6), p.1967-1979</ispartof><rights>The Author(s), under exclusive licence to Springer Nature Limited 2020</rights><rights>COPYRIGHT 2021 Nature Publishing Group</rights><rights>The Author(s), under exclusive licence to Springer Nature Limited 2020.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c603t-1e3ddc5b26dbf1ef6bc1d8ec8b09524f89bb20deff07c2201d420fed07a40d5a3</citedby><cites>FETCH-LOGICAL-c603t-1e3ddc5b26dbf1ef6bc1d8ec8b09524f89bb20deff07c2201d420fed07a40d5a3</cites><orcidid>0000-0002-9202-4469 ; 0000-0002-3519-9596</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41380-020-0693-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41380-020-0693-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32099100$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rein, Benjamin</creatorcontrib><creatorcontrib>Tan, Tao</creatorcontrib><creatorcontrib>Yang, Fengwei</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Williams, Jamal</creatorcontrib><creatorcontrib>Zhang, Freddy</creatorcontrib><creatorcontrib>Mills, Alea</creatorcontrib><creatorcontrib>Yan, Zhen</creatorcontrib><title>Reversal of synaptic and behavioral deficits in a 16p11.2 duplication mouse model via restoration of the GABA synapse regulator Npas4</title><title>Molecular psychiatry</title><addtitle>Mol Psychiatry</addtitle><addtitle>Mol Psychiatry</addtitle><description>The human 16p11.2 gene locus is a hot spot for copy number variations, which predispose carriers to a range of neuropsychiatric phenotypes. Microduplications of 16p11.2 are associated with autism spectrum disorder (ASD), intellectual disability (ID), and schizophrenia (SZ). Despite the debilitating nature of 16p11.2 duplications, the underlying molecular mechanisms remain poorly understood. Here we performed a comprehensive behavioral characterization of 16p11.2 duplication mice (16p11.2
dp/+
) and identified social and cognitive deficits reminiscent of ASD and ID phenotypes. 16p11.2
dp/+
mice did not exhibit the SZ-related sensorimotor gating deficits, psychostimulant-induced hypersensitivity, or motor impairment. Electrophysiological recordings of 16p11.2
dp/+
mice found deficient GABAergic synaptic transmission and elevated neuronal excitability in the prefrontal cortex (PFC), a brain region critical for social and cognitive functions. RNA-sequencing identified genome-wide transcriptional aberrance in the PFC of 16p11.2
dp/+
mice, including downregulation of the GABA synapse regulator
Npas4
. Restoring
Npas4
expression in PFC of 16p11.2
dp/+
mice ameliorated the social and cognitive deficits and reversed GABAergic synaptic impairment and neuronal hyperexcitability. These findings suggest that prefrontal cortical GABAergic synaptic circuitry and Npas4 are strongly implicated in 16p11.2 duplication pathology, and may represent potential targets for therapeutic intervention in ASD.</description><subject>13/89</subject><subject>38/39</subject><subject>38/77</subject><subject>45/91</subject><subject>631/378</subject><subject>692/699/476/1373</subject><subject>9/74</subject><subject>Autism</subject><subject>Behavioral Sciences</subject><subject>Biological Psychology</subject><subject>Care and treatment</subject><subject>Chromosome 16</subject><subject>Cognitive ability</subject><subject>Copy number</subject><subject>Copy number variations</subject><subject>Development and progression</subject><subject>Excitability</subject><subject>GABA</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Hypersensitivity</subject><subject>Intellectual disabilities</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mental disorders</subject><subject>Molecular modelling</subject><subject>Mutation hot spots</subject><subject>Neurosciences</subject><subject>Neurotransmitters</subject><subject>Pervasive developmental disorders</subject><subject>Pharmacotherapy</subject><subject>Phenotypes</subject><subject>Physiological aspects</subject><subject>Prefrontal cortex</subject><subject>Psychiatry</subject><subject>Schizophrenia</subject><subject>Sensorimotor gating</subject><subject>Synapses</subject><subject>Synaptic transmission</subject><subject>Transcription</subject><subject>Transcription factors</subject><subject>γ-Aminobutyric 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deficits in a 16p11.2 duplication mouse model via restoration of the GABA synapse regulator Npas4</title><author>Rein, Benjamin ; Tan, Tao ; Yang, Fengwei ; Wang, Wei ; Williams, Jamal ; Zhang, Freddy ; Mills, Alea ; Yan, Zhen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c603t-1e3ddc5b26dbf1ef6bc1d8ec8b09524f89bb20deff07c2201d420fed07a40d5a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>13/89</topic><topic>38/39</topic><topic>38/77</topic><topic>45/91</topic><topic>631/378</topic><topic>692/699/476/1373</topic><topic>9/74</topic><topic>Autism</topic><topic>Behavioral Sciences</topic><topic>Biological Psychology</topic><topic>Care and treatment</topic><topic>Chromosome 16</topic><topic>Cognitive ability</topic><topic>Copy number</topic><topic>Copy number variations</topic><topic>Development and progression</topic><topic>Excitability</topic><topic>GABA</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Health aspects</topic><topic>Hypersensitivity</topic><topic>Intellectual disabilities</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mental disorders</topic><topic>Molecular modelling</topic><topic>Mutation hot spots</topic><topic>Neurosciences</topic><topic>Neurotransmitters</topic><topic>Pervasive developmental disorders</topic><topic>Pharmacotherapy</topic><topic>Phenotypes</topic><topic>Physiological aspects</topic><topic>Prefrontal cortex</topic><topic>Psychiatry</topic><topic>Schizophrenia</topic><topic>Sensorimotor gating</topic><topic>Synapses</topic><topic>Synaptic transmission</topic><topic>Transcription</topic><topic>Transcription factors</topic><topic>γ-Aminobutyric acid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rein, Benjamin</creatorcontrib><creatorcontrib>Tan, Tao</creatorcontrib><creatorcontrib>Yang, Fengwei</creatorcontrib><creatorcontrib>Wang, Wei</creatorcontrib><creatorcontrib>Williams, Jamal</creatorcontrib><creatorcontrib>Zhang, Freddy</creatorcontrib><creatorcontrib>Mills, Alea</creatorcontrib><creatorcontrib>Yan, Zhen</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central 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Npas4</atitle><jtitle>Molecular psychiatry</jtitle><stitle>Mol Psychiatry</stitle><addtitle>Mol Psychiatry</addtitle><date>2021-06-01</date><risdate>2021</risdate><volume>26</volume><issue>6</issue><spage>1967</spage><epage>1979</epage><pages>1967-1979</pages><issn>1359-4184</issn><eissn>1476-5578</eissn><abstract>The human 16p11.2 gene locus is a hot spot for copy number variations, which predispose carriers to a range of neuropsychiatric phenotypes. Microduplications of 16p11.2 are associated with autism spectrum disorder (ASD), intellectual disability (ID), and schizophrenia (SZ). Despite the debilitating nature of 16p11.2 duplications, the underlying molecular mechanisms remain poorly understood. Here we performed a comprehensive behavioral characterization of 16p11.2 duplication mice (16p11.2
dp/+
) and identified social and cognitive deficits reminiscent of ASD and ID phenotypes. 16p11.2
dp/+
mice did not exhibit the SZ-related sensorimotor gating deficits, psychostimulant-induced hypersensitivity, or motor impairment. Electrophysiological recordings of 16p11.2
dp/+
mice found deficient GABAergic synaptic transmission and elevated neuronal excitability in the prefrontal cortex (PFC), a brain region critical for social and cognitive functions. RNA-sequencing identified genome-wide transcriptional aberrance in the PFC of 16p11.2
dp/+
mice, including downregulation of the GABA synapse regulator
Npas4
. Restoring
Npas4
expression in PFC of 16p11.2
dp/+
mice ameliorated the social and cognitive deficits and reversed GABAergic synaptic impairment and neuronal hyperexcitability. These findings suggest that prefrontal cortical GABAergic synaptic circuitry and Npas4 are strongly implicated in 16p11.2 duplication pathology, and may represent potential targets for therapeutic intervention in ASD.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>32099100</pmid><doi>10.1038/s41380-020-0693-9</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0002-9202-4469</orcidid><orcidid>https://orcid.org/0000-0002-3519-9596</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Molecular psychiatry, 2021-06, Vol.26 (6), p.1967-1979 |
| issn | 1359-4184 1476-5578 |
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| source | SpringerLink Journals - AutoHoldings |
| subjects | 13/89 38/39 38/77 45/91 631/378 692/699/476/1373 9/74 Autism Behavioral Sciences Biological Psychology Care and treatment Chromosome 16 Cognitive ability Copy number Copy number variations Development and progression Excitability GABA Genetic aspects Genomes Health aspects Hypersensitivity Intellectual disabilities Medicine Medicine & Public Health Mental disorders Molecular modelling Mutation hot spots Neurosciences Neurotransmitters Pervasive developmental disorders Pharmacotherapy Phenotypes Physiological aspects Prefrontal cortex Psychiatry Schizophrenia Sensorimotor gating Synapses Synaptic transmission Transcription Transcription factors γ-Aminobutyric acid |
| title | Reversal of synaptic and behavioral deficits in a 16p11.2 duplication mouse model via restoration of the GABA synapse regulator Npas4 |
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