Shared Synaptic Pathophysiology in Syndromic and Nonsyndromic Rodent Models of Autism
The genetic heterogeneity of autism poses a major challenge for identifying mechanism-based treatments. A number of rare mutations are associated with autism, and it is unclear whether these result in common neuronal alterations. Monogenic syndromes, such as fragile X, include autism as one of their...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2012-10, Vol.338 (6103), p.128-132 |
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| creator | Baudouin, Stéphane J. Gaudias, Julien Gerharz, Stefan Hatstatt, Laetitia Zhou, Kuikui Punnakkal, Pradeep Tanaka, Kenji F. Spooren, Will Hen, Rene De Zeeuw, Chris I. Vogt, Kaspar Scheiffele, Peter |
| description | The genetic heterogeneity of autism poses a major challenge for identifying mechanism-based treatments. A number of rare mutations are associated with autism, and it is unclear whether these result in common neuronal alterations. Monogenic syndromes, such as fragile X, include autism as one of their multifaceted symptoms and have revealed specific defects in synaptic plasticity. We discovered an unexpected convergence of synaptic pathophysiology in a nonsyndromic form of autism with those in fragile X syndrome. Neuroligin-3 knockout mice (a model for nonsyndromic autism) exhibited disrupted heterosynaptic competition and perturbed metabotropic glutamate receptor—dependent synaptic plasticity, a hallmark of fragile X. These phenotypes could be rescued by reexpression of neuroligin-3 in juvenile mice, highlighting the possibility of reverting neuronal circuit alterations in autism after the completion of development. |
| doi_str_mv | 10.1126/science.1224159 |
| format | Article |
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A number of rare mutations are associated with autism, and it is unclear whether these result in common neuronal alterations. Monogenic syndromes, such as fragile X, include autism as one of their multifaceted symptoms and have revealed specific defects in synaptic plasticity. We discovered an unexpected convergence of synaptic pathophysiology in a nonsyndromic form of autism with those in fragile X syndrome. Neuroligin-3 knockout mice (a model for nonsyndromic autism) exhibited disrupted heterosynaptic competition and perturbed metabotropic glutamate receptor—dependent synaptic plasticity, a hallmark of fragile X. These phenotypes could be rescued by reexpression of neuroligin-3 in juvenile mice, highlighting the possibility of reverting neuronal circuit alterations in autism after the completion of development.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.1224159</identifier><identifier>PMID: 22983708</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Association for the Advancement of Science</publisher><subject>Animals ; Autism ; Autistic disorder ; Autistic Disorder - physiopathology ; Behavioral neuroscience ; Biological and medical sciences ; Cell Adhesion Molecules, Neuronal - genetics ; Cell Adhesion Molecules, Neuronal - metabolism ; Cerebellum ; Chromosome fragility (bloom syndrome, ataxia telangiectasia, fanconi anemia, x-linked mental retardation...) ; Disease Models, Animal ; Fragile X syndrome ; Fragile X Syndrome - genetics ; Fragile X Syndrome - physiopathology ; Fundamental and applied biological sciences. Psychology ; Genetics ; Genotype & phenotype ; Male ; Medical genetics ; Medical sciences ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular biology ; Mutation ; Nerve Net - metabolism ; Nerve Net - physiopathology ; Nerve Net - ultrastructure ; Nerve Tissue Proteins - genetics ; Nerve Tissue Proteins - metabolism ; Neuronal Plasticity ; Neurons ; Neurotransmitters ; Phenotypes ; Rodents ; Social interaction ; Synapses ; Synapses - metabolism ; Synapses - physiology ; Synapses - ultrastructure ; T tests ; Vertebrates: nervous system and sense organs</subject><ispartof>Science (American Association for the Advancement of Science), 2012-10, Vol.338 (6103), p.128-132</ispartof><rights>Copyright © 2012 American Association for the Advancement of Science</rights><rights>2014 INIST-CNRS</rights><rights>Copyright © 2012, American Association for the Advancement of Science</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c517t-a5baf9638ab3ebdca9d91cba81ef89d363b2aa757b4644ee103e44453e0b71903</citedby><cites>FETCH-LOGICAL-c517t-a5baf9638ab3ebdca9d91cba81ef89d363b2aa757b4644ee103e44453e0b71903</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/41704048$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/41704048$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,2871,2872,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26691265$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22983708$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Baudouin, Stéphane J.</creatorcontrib><creatorcontrib>Gaudias, Julien</creatorcontrib><creatorcontrib>Gerharz, Stefan</creatorcontrib><creatorcontrib>Hatstatt, Laetitia</creatorcontrib><creatorcontrib>Zhou, Kuikui</creatorcontrib><creatorcontrib>Punnakkal, Pradeep</creatorcontrib><creatorcontrib>Tanaka, Kenji F.</creatorcontrib><creatorcontrib>Spooren, Will</creatorcontrib><creatorcontrib>Hen, Rene</creatorcontrib><creatorcontrib>De Zeeuw, Chris I.</creatorcontrib><creatorcontrib>Vogt, Kaspar</creatorcontrib><creatorcontrib>Scheiffele, Peter</creatorcontrib><title>Shared Synaptic Pathophysiology in Syndromic and Nonsyndromic Rodent Models of Autism</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>The genetic heterogeneity of autism poses a major challenge for identifying mechanism-based treatments. A number of rare mutations are associated with autism, and it is unclear whether these result in common neuronal alterations. Monogenic syndromes, such as fragile X, include autism as one of their multifaceted symptoms and have revealed specific defects in synaptic plasticity. We discovered an unexpected convergence of synaptic pathophysiology in a nonsyndromic form of autism with those in fragile X syndrome. Neuroligin-3 knockout mice (a model for nonsyndromic autism) exhibited disrupted heterosynaptic competition and perturbed metabotropic glutamate receptor—dependent synaptic plasticity, a hallmark of fragile X. These phenotypes could be rescued by reexpression of neuroligin-3 in juvenile mice, highlighting the possibility of reverting neuronal circuit alterations in autism after the completion of development.</description><subject>Animals</subject><subject>Autism</subject><subject>Autistic disorder</subject><subject>Autistic Disorder - physiopathology</subject><subject>Behavioral neuroscience</subject><subject>Biological and medical sciences</subject><subject>Cell Adhesion Molecules, Neuronal - genetics</subject><subject>Cell Adhesion Molecules, Neuronal - metabolism</subject><subject>Cerebellum</subject><subject>Chromosome fragility (bloom syndrome, ataxia telangiectasia, fanconi anemia, x-linked mental retardation...)</subject><subject>Disease Models, Animal</subject><subject>Fragile X syndrome</subject><subject>Fragile X Syndrome - genetics</subject><subject>Fragile X Syndrome - physiopathology</subject><subject>Fundamental and applied biological sciences. 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Academic</collection><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Baudouin, Stéphane J.</au><au>Gaudias, Julien</au><au>Gerharz, Stefan</au><au>Hatstatt, Laetitia</au><au>Zhou, Kuikui</au><au>Punnakkal, Pradeep</au><au>Tanaka, Kenji F.</au><au>Spooren, Will</au><au>Hen, Rene</au><au>De Zeeuw, Chris I.</au><au>Vogt, Kaspar</au><au>Scheiffele, Peter</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Shared Synaptic Pathophysiology in Syndromic and Nonsyndromic Rodent Models of Autism</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>2012-10-05</date><risdate>2012</risdate><volume>338</volume><issue>6103</issue><spage>128</spage><epage>132</epage><pages>128-132</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><coden>SCIEAS</coden><abstract>The genetic heterogeneity of autism poses a major challenge for identifying mechanism-based treatments. A number of rare mutations are associated with autism, and it is unclear whether these result in common neuronal alterations. Monogenic syndromes, such as fragile X, include autism as one of their multifaceted symptoms and have revealed specific defects in synaptic plasticity. We discovered an unexpected convergence of synaptic pathophysiology in a nonsyndromic form of autism with those in fragile X syndrome. Neuroligin-3 knockout mice (a model for nonsyndromic autism) exhibited disrupted heterosynaptic competition and perturbed metabotropic glutamate receptor—dependent synaptic plasticity, a hallmark of fragile X. These phenotypes could be rescued by reexpression of neuroligin-3 in juvenile mice, highlighting the possibility of reverting neuronal circuit alterations in autism after the completion of development.</abstract><cop>Washington, DC</cop><pub>American Association for the Advancement of Science</pub><pmid>22983708</pmid><doi>10.1126/science.1224159</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| source | American Association for the Advancement of Science; Jstor Complete Legacy; MEDLINE |
| subjects | Animals Autism Autistic disorder Autistic Disorder - physiopathology Behavioral neuroscience Biological and medical sciences Cell Adhesion Molecules, Neuronal - genetics Cell Adhesion Molecules, Neuronal - metabolism Cerebellum Chromosome fragility (bloom syndrome, ataxia telangiectasia, fanconi anemia, x-linked mental retardation...) Disease Models, Animal Fragile X syndrome Fragile X Syndrome - genetics Fragile X Syndrome - physiopathology Fundamental and applied biological sciences. Psychology Genetics Genotype & phenotype Male Medical genetics Medical sciences Membrane Proteins - genetics Membrane Proteins - metabolism Mice Mice, Inbred C57BL Mice, Knockout Molecular biology Mutation Nerve Net - metabolism Nerve Net - physiopathology Nerve Net - ultrastructure Nerve Tissue Proteins - genetics Nerve Tissue Proteins - metabolism Neuronal Plasticity Neurons Neurotransmitters Phenotypes Rodents Social interaction Synapses Synapses - metabolism Synapses - physiology Synapses - ultrastructure T tests Vertebrates: nervous system and sense organs |
| title | Shared Synaptic Pathophysiology in Syndromic and Nonsyndromic Rodent Models of Autism |
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