β‐adducin (Add2) KO mice show synaptic plasticity, motor coordination and behavioral deficits accompanied by changes in the expression and phosphorylation levels of the α‐ and γ‐adducin subunits
Adducins are a family of proteins found in cytoskeleton junctional complexes, which bind and regulate actin filaments and actin‐spectrin complexes. In brain, adducin is expressed at high levels and is identified as a constituent of synaptic structures, such as dendritic spines and growth cones of ne...
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Veröffentlicht in: | Genes, brain and behavior brain and behavior, 2010-02, Vol.9 (1), p.84-96 |
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description | Adducins are a family of proteins found in cytoskeleton junctional complexes, which bind and regulate actin filaments and actin‐spectrin complexes. In brain, adducin is expressed at high levels and is identified as a constituent of synaptic structures, such as dendritic spines and growth cones of neurons. Adducin‐induced changes in dendritic spines are involved in activity‐dependent synaptic plasticity processes associated with learning and memory, but the mechanisms underlying these functions remain to be elucidated. Here, β‐adducin knockout (KO) mice were used to obtain a deeper insight into the role of adducin in these processes. We showed that β‐adducin KO mice showed behavioral, motor coordination and learning deficits together with an altered expression and/or phosphorylation levels of α‐adducin and γ‐adducin. We found that β‐adducin KO mice exhibited deficits in learning and motor performances associated with an impairment of long‐term potentiation (LTP) and long‐term depression (LTD) in the hippocampus. These effects were accompanied by a decrease in phosphorylation of adducin, a reduction in α‐adducin expression levels and upregulation of γ‐adducin in hippocampus, cerebellum and neocortex of mutant mice. In addition, we found that the mRNA encoding β‐adducin is also located in dendrites, where it may participate in the fine modulation of LTP and LTD. These results strongly suggest coordinated expression and phosphorylation of adducin subunits as a key mechanism underlying synaptic plasticity, motor coordination performance and learning behaviors. |
doi_str_mv | 10.1111/j.1601-183X.2009.00537.x |
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F.</creator><creatorcontrib>Porro, F. ; Rosato‐Siri, M. ; Leone, E. ; Costessi, L. ; Iaconcig, A. ; Tongiorgi, E. ; Muro, A. F.</creatorcontrib><description>Adducins are a family of proteins found in cytoskeleton junctional complexes, which bind and regulate actin filaments and actin‐spectrin complexes. In brain, adducin is expressed at high levels and is identified as a constituent of synaptic structures, such as dendritic spines and growth cones of neurons. Adducin‐induced changes in dendritic spines are involved in activity‐dependent synaptic plasticity processes associated with learning and memory, but the mechanisms underlying these functions remain to be elucidated. Here, β‐adducin knockout (KO) mice were used to obtain a deeper insight into the role of adducin in these processes. We showed that β‐adducin KO mice showed behavioral, motor coordination and learning deficits together with an altered expression and/or phosphorylation levels of α‐adducin and γ‐adducin. We found that β‐adducin KO mice exhibited deficits in learning and motor performances associated with an impairment of long‐term potentiation (LTP) and long‐term depression (LTD) in the hippocampus. These effects were accompanied by a decrease in phosphorylation of adducin, a reduction in α‐adducin expression levels and upregulation of γ‐adducin in hippocampus, cerebellum and neocortex of mutant mice. In addition, we found that the mRNA encoding β‐adducin is also located in dendrites, where it may participate in the fine modulation of LTP and LTD. These results strongly suggest coordinated expression and phosphorylation of adducin subunits as a key mechanism underlying synaptic plasticity, motor coordination performance and learning behaviors.</description><identifier>ISSN: 1601-1848</identifier><identifier>EISSN: 1601-183X</identifier><identifier>DOI: 10.1111/j.1601-183X.2009.00537.x</identifier><identifier>PMID: 19900187</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Behavior ; Behavior, Animal - physiology ; Calmodulin-Binding Proteins - deficiency ; Calmodulin-Binding Proteins - genetics ; Calmodulin-Binding Proteins - metabolism ; cytoskeleton ; Dendrites - physiology ; Learning Disorders - etiology ; Long-Term Potentiation ; Long-Term Synaptic Depression ; LTD ; LTP ; Mental Disorders - etiology ; Mice ; Mice, Knockout ; Motor Skills - physiology ; Motor Skills Disorders - etiology ; Neuronal Plasticity - physiology ; Phosphorylation ; RNA, Messenger - metabolism ; somatodendritic localization ; Synapses - physiology</subject><ispartof>Genes, brain and behavior, 2010-02, Vol.9 (1), p.84-96</ispartof><rights>2009 International Centre for Genetic Engineering and Biotechnology. 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F.</creatorcontrib><title>β‐adducin (Add2) KO mice show synaptic plasticity, motor coordination and behavioral deficits accompanied by changes in the expression and phosphorylation levels of the α‐ and γ‐adducin subunits</title><title>Genes, brain and behavior</title><addtitle>Genes Brain Behav</addtitle><description>Adducins are a family of proteins found in cytoskeleton junctional complexes, which bind and regulate actin filaments and actin‐spectrin complexes. In brain, adducin is expressed at high levels and is identified as a constituent of synaptic structures, such as dendritic spines and growth cones of neurons. Adducin‐induced changes in dendritic spines are involved in activity‐dependent synaptic plasticity processes associated with learning and memory, but the mechanisms underlying these functions remain to be elucidated. Here, β‐adducin knockout (KO) mice were used to obtain a deeper insight into the role of adducin in these processes. We showed that β‐adducin KO mice showed behavioral, motor coordination and learning deficits together with an altered expression and/or phosphorylation levels of α‐adducin and γ‐adducin. We found that β‐adducin KO mice exhibited deficits in learning and motor performances associated with an impairment of long‐term potentiation (LTP) and long‐term depression (LTD) in the hippocampus. These effects were accompanied by a decrease in phosphorylation of adducin, a reduction in α‐adducin expression levels and upregulation of γ‐adducin in hippocampus, cerebellum and neocortex of mutant mice. In addition, we found that the mRNA encoding β‐adducin is also located in dendrites, where it may participate in the fine modulation of LTP and LTD. These results strongly suggest coordinated expression and phosphorylation of adducin subunits as a key mechanism underlying synaptic plasticity, motor coordination performance and learning behaviors.</description><subject>Animals</subject><subject>Behavior</subject><subject>Behavior, Animal - physiology</subject><subject>Calmodulin-Binding Proteins - deficiency</subject><subject>Calmodulin-Binding Proteins - genetics</subject><subject>Calmodulin-Binding Proteins - metabolism</subject><subject>cytoskeleton</subject><subject>Dendrites - physiology</subject><subject>Learning Disorders - etiology</subject><subject>Long-Term Potentiation</subject><subject>Long-Term Synaptic Depression</subject><subject>LTD</subject><subject>LTP</subject><subject>Mental Disorders - etiology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Motor Skills - physiology</subject><subject>Motor Skills Disorders - etiology</subject><subject>Neuronal Plasticity - physiology</subject><subject>Phosphorylation</subject><subject>RNA, Messenger - metabolism</subject><subject>somatodendritic localization</subject><subject>Synapses - physiology</subject><issn>1601-1848</issn><issn>1601-183X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc9u1DAQxiMEoqXwCsg3QGKDHTv_JC5tBQVRqReQuFmOPSFeOXawk3Zz4xF4FeAxkPYheBKc3aVwxLI1Y_k334z8JQkiOCVxvVinpMBkRSr6Mc0wrlOMc1qmmzvJ8e3D3ducVUfJgxDWGJOSVuR-ckTqOl6q8jj5uf3-68tXodQktUVPT5XKnqF3V6jXElDo3A0KsxXDqCUajAgx6nF-jno3Oo-kc15pK0btLBJWoQY6ca2dFwYpaBc2ICGl6wdhNcT3GclO2E8QUOw2doBgM3gI4Y_A0LkQj5_NXtTANZiAXLuDt9_irDtu--OfqcPUTDa2epjca4UJ8OgQT5IPr1-9P3-zury6eHt-ermSLMvKlWjyqgBaMlrURNWUFSDythK0lEzJJu42J1lREVIwIQjO2obVMqdNWdSNYhk9SZ7sdQfvPk8QRt7rIMEYYcFNgZeU1ix-9UJWe1J6F4KHlg9e98LPnGC-OMnXfDGJL4bxxUm-c5JvYunjQ5Op6UH9LTxYF4GXe-BGG5j_W5hfnJ3FhP4GeaW2Hg</recordid><startdate>201002</startdate><enddate>201002</enddate><creator>Porro, F.</creator><creator>Rosato‐Siri, M.</creator><creator>Leone, E.</creator><creator>Costessi, L.</creator><creator>Iaconcig, A.</creator><creator>Tongiorgi, E.</creator><creator>Muro, A. 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F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>β‐adducin (Add2) KO mice show synaptic plasticity, motor coordination and behavioral deficits accompanied by changes in the expression and phosphorylation levels of the α‐ and γ‐adducin subunits</atitle><jtitle>Genes, brain and behavior</jtitle><addtitle>Genes Brain Behav</addtitle><date>2010-02</date><risdate>2010</risdate><volume>9</volume><issue>1</issue><spage>84</spage><epage>96</epage><pages>84-96</pages><issn>1601-1848</issn><eissn>1601-183X</eissn><abstract>Adducins are a family of proteins found in cytoskeleton junctional complexes, which bind and regulate actin filaments and actin‐spectrin complexes. In brain, adducin is expressed at high levels and is identified as a constituent of synaptic structures, such as dendritic spines and growth cones of neurons. Adducin‐induced changes in dendritic spines are involved in activity‐dependent synaptic plasticity processes associated with learning and memory, but the mechanisms underlying these functions remain to be elucidated. Here, β‐adducin knockout (KO) mice were used to obtain a deeper insight into the role of adducin in these processes. We showed that β‐adducin KO mice showed behavioral, motor coordination and learning deficits together with an altered expression and/or phosphorylation levels of α‐adducin and γ‐adducin. We found that β‐adducin KO mice exhibited deficits in learning and motor performances associated with an impairment of long‐term potentiation (LTP) and long‐term depression (LTD) in the hippocampus. These effects were accompanied by a decrease in phosphorylation of adducin, a reduction in α‐adducin expression levels and upregulation of γ‐adducin in hippocampus, cerebellum and neocortex of mutant mice. 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subjects | Animals Behavior Behavior, Animal - physiology Calmodulin-Binding Proteins - deficiency Calmodulin-Binding Proteins - genetics Calmodulin-Binding Proteins - metabolism cytoskeleton Dendrites - physiology Learning Disorders - etiology Long-Term Potentiation Long-Term Synaptic Depression LTD LTP Mental Disorders - etiology Mice Mice, Knockout Motor Skills - physiology Motor Skills Disorders - etiology Neuronal Plasticity - physiology Phosphorylation RNA, Messenger - metabolism somatodendritic localization Synapses - physiology |
title | β‐adducin (Add2) KO mice show synaptic plasticity, motor coordination and behavioral deficits accompanied by changes in the expression and phosphorylation levels of the α‐ and γ‐adducin subunits |
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