Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity
Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Menna, Elisabetta [verfasserIn] Zambetti, Stefania [verfasserIn] Morini, Raffaella [verfasserIn] Donzelli, Andrea [verfasserIn] Disanza, Andrea [verfasserIn] Calvigioni, Daniela [verfasserIn] Braida, Daniela [verfasserIn] Nicolini, Chiara [verfasserIn] Orlando, Marta [verfasserIn] Fossati, Giuliana [verfasserIn] Cristina Regondi, Maria [verfasserIn] Pattini, Linda [verfasserIn] Frassoni, Carolina [verfasserIn] Francolini, Maura [verfasserIn] Scita, Giorgio [verfasserIn] Sala, Mariaelvina [verfasserIn] Fahnestock, Margaret [verfasserIn] Matteoli, Michela [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2013 |
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| Schlagwörter: |
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| Anmerkung: |
© European Molecular Biology Organization 2013 |
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| Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 32(2013), 12 vom: 17. Mai, Seite 1730-1744 |
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| Übergeordnetes Werk: |
volume:32 ; year:2013 ; number:12 ; day:17 ; month:05 ; pages:1730-1744 |
| Links: |
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| DOI / URN: |
10.1038/emboj.2013.107 |
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| Katalog-ID: |
SPR057868689 |
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| 100 | 1 | |a Menna, Elisabetta |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity |
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| 520 | |a Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape and synaptic strength and, consistently, abnormalities in spine number and morphology have been described in a number of neurological disorders. In the present study, we demonstrate that the actin‐regulating protein, Eps8, is recruited to the spine head during chemically induced long‐term potentiation in culture and that inhibition of its actin‐capping activity impairs spine enlargement and plasticity. Accordingly, mice lacking Eps8 display immature spines, which are unable to undergo potentiation, and are impaired in cognitive functions. Additionally, we found that reduction in the levels of Eps8 occurs in brains of patients affected by autism compared to controls. Our data reveal the key role of Eps8 actin‐capping activity in spine morphogenesis and plasticity and indicate that reductions in actin‐capping proteins may characterize forms of intellectual disabilities associated with spine defects. | ||
| 520 | |a Abstract Reduced Eps8 levels in brains of autism patients correlate with impaired spine morphogenesis and cognitive function in Eps8‐deficient mice, suggesting causal links between actin‐remodelling defects and certain intellectual disabilities. | ||
| 650 | 4 | |a actin‐capping activity |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a activity‐dependent plasticity |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Eps8 |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a learning and memory defects |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a spine morphogenesis |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Zambetti, Stefania |e verfasserin |4 aut | |
| 700 | 1 | |a Morini, Raffaella |e verfasserin |4 aut | |
| 700 | 1 | |a Donzelli, Andrea |e verfasserin |4 aut | |
| 700 | 1 | |a Disanza, Andrea |e verfasserin |4 aut | |
| 700 | 1 | |a Calvigioni, Daniela |e verfasserin |4 aut | |
| 700 | 1 | |a Braida, Daniela |e verfasserin |4 aut | |
| 700 | 1 | |a Nicolini, Chiara |e verfasserin |4 aut | |
| 700 | 1 | |a Orlando, Marta |e verfasserin |4 aut | |
| 700 | 1 | |a Fossati, Giuliana |e verfasserin |4 aut | |
| 700 | 1 | |a Cristina Regondi, Maria |e verfasserin |4 aut | |
| 700 | 1 | |a Pattini, Linda |e verfasserin |4 aut | |
| 700 | 1 | |a Frassoni, Carolina |e verfasserin |4 aut | |
| 700 | 1 | |a Francolini, Maura |e verfasserin |4 aut | |
| 700 | 1 | |a Scita, Giorgio |e verfasserin |4 aut | |
| 700 | 1 | |a Sala, Mariaelvina |e verfasserin |4 aut | |
| 700 | 1 | |a Fahnestock, Margaret |e verfasserin |4 aut | |
| 700 | 1 | |a Matteoli, Michela |e verfasserin |4 aut | |
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10.1038/emboj.2013.107 doi (DE-627)SPR057868689 (SPR)emboj.2013.107-e DE-627 ger DE-627 rakwb eng Menna, Elisabetta verfasserin aut Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2013 Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape and synaptic strength and, consistently, abnormalities in spine number and morphology have been described in a number of neurological disorders. In the present study, we demonstrate that the actin‐regulating protein, Eps8, is recruited to the spine head during chemically induced long‐term potentiation in culture and that inhibition of its actin‐capping activity impairs spine enlargement and plasticity. Accordingly, mice lacking Eps8 display immature spines, which are unable to undergo potentiation, and are impaired in cognitive functions. Additionally, we found that reduction in the levels of Eps8 occurs in brains of patients affected by autism compared to controls. Our data reveal the key role of Eps8 actin‐capping activity in spine morphogenesis and plasticity and indicate that reductions in actin‐capping proteins may characterize forms of intellectual disabilities associated with spine defects. Abstract Reduced Eps8 levels in brains of autism patients correlate with impaired spine morphogenesis and cognitive function in Eps8‐deficient mice, suggesting causal links between actin‐remodelling defects and certain intellectual disabilities. actin‐capping activity (dpeaa)DE-He213 activity‐dependent plasticity (dpeaa)DE-He213 Eps8 (dpeaa)DE-He213 learning and memory defects (dpeaa)DE-He213 spine morphogenesis (dpeaa)DE-He213 Zambetti, Stefania verfasserin aut Morini, Raffaella verfasserin aut Donzelli, Andrea verfasserin aut Disanza, Andrea verfasserin aut Calvigioni, Daniela verfasserin aut Braida, Daniela verfasserin aut Nicolini, Chiara verfasserin aut Orlando, Marta verfasserin aut Fossati, Giuliana verfasserin aut Cristina Regondi, Maria verfasserin aut Pattini, Linda verfasserin aut Frassoni, Carolina verfasserin aut Francolini, Maura verfasserin aut Scita, Giorgio verfasserin aut Sala, Mariaelvina verfasserin aut Fahnestock, Margaret verfasserin aut Matteoli, Michela verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 32(2013), 12 vom: 17. Mai, Seite 1730-1744 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:32 year:2013 number:12 day:17 month:05 pages:1730-1744 https://dx.doi.org/10.1038/emboj.2013.107 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 32 2013 12 17 05 1730-1744 |
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10.1038/emboj.2013.107 doi (DE-627)SPR057868689 (SPR)emboj.2013.107-e DE-627 ger DE-627 rakwb eng Menna, Elisabetta verfasserin aut Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2013 Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape and synaptic strength and, consistently, abnormalities in spine number and morphology have been described in a number of neurological disorders. In the present study, we demonstrate that the actin‐regulating protein, Eps8, is recruited to the spine head during chemically induced long‐term potentiation in culture and that inhibition of its actin‐capping activity impairs spine enlargement and plasticity. Accordingly, mice lacking Eps8 display immature spines, which are unable to undergo potentiation, and are impaired in cognitive functions. Additionally, we found that reduction in the levels of Eps8 occurs in brains of patients affected by autism compared to controls. Our data reveal the key role of Eps8 actin‐capping activity in spine morphogenesis and plasticity and indicate that reductions in actin‐capping proteins may characterize forms of intellectual disabilities associated with spine defects. Abstract Reduced Eps8 levels in brains of autism patients correlate with impaired spine morphogenesis and cognitive function in Eps8‐deficient mice, suggesting causal links between actin‐remodelling defects and certain intellectual disabilities. actin‐capping activity (dpeaa)DE-He213 activity‐dependent plasticity (dpeaa)DE-He213 Eps8 (dpeaa)DE-He213 learning and memory defects (dpeaa)DE-He213 spine morphogenesis (dpeaa)DE-He213 Zambetti, Stefania verfasserin aut Morini, Raffaella verfasserin aut Donzelli, Andrea verfasserin aut Disanza, Andrea verfasserin aut Calvigioni, Daniela verfasserin aut Braida, Daniela verfasserin aut Nicolini, Chiara verfasserin aut Orlando, Marta verfasserin aut Fossati, Giuliana verfasserin aut Cristina Regondi, Maria verfasserin aut Pattini, Linda verfasserin aut Frassoni, Carolina verfasserin aut Francolini, Maura verfasserin aut Scita, Giorgio verfasserin aut Sala, Mariaelvina verfasserin aut Fahnestock, Margaret verfasserin aut Matteoli, Michela verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 32(2013), 12 vom: 17. Mai, Seite 1730-1744 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:32 year:2013 number:12 day:17 month:05 pages:1730-1744 https://dx.doi.org/10.1038/emboj.2013.107 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 32 2013 12 17 05 1730-1744 |
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10.1038/emboj.2013.107 doi (DE-627)SPR057868689 (SPR)emboj.2013.107-e DE-627 ger DE-627 rakwb eng Menna, Elisabetta verfasserin aut Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2013 Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape and synaptic strength and, consistently, abnormalities in spine number and morphology have been described in a number of neurological disorders. In the present study, we demonstrate that the actin‐regulating protein, Eps8, is recruited to the spine head during chemically induced long‐term potentiation in culture and that inhibition of its actin‐capping activity impairs spine enlargement and plasticity. Accordingly, mice lacking Eps8 display immature spines, which are unable to undergo potentiation, and are impaired in cognitive functions. Additionally, we found that reduction in the levels of Eps8 occurs in brains of patients affected by autism compared to controls. Our data reveal the key role of Eps8 actin‐capping activity in spine morphogenesis and plasticity and indicate that reductions in actin‐capping proteins may characterize forms of intellectual disabilities associated with spine defects. Abstract Reduced Eps8 levels in brains of autism patients correlate with impaired spine morphogenesis and cognitive function in Eps8‐deficient mice, suggesting causal links between actin‐remodelling defects and certain intellectual disabilities. actin‐capping activity (dpeaa)DE-He213 activity‐dependent plasticity (dpeaa)DE-He213 Eps8 (dpeaa)DE-He213 learning and memory defects (dpeaa)DE-He213 spine morphogenesis (dpeaa)DE-He213 Zambetti, Stefania verfasserin aut Morini, Raffaella verfasserin aut Donzelli, Andrea verfasserin aut Disanza, Andrea verfasserin aut Calvigioni, Daniela verfasserin aut Braida, Daniela verfasserin aut Nicolini, Chiara verfasserin aut Orlando, Marta verfasserin aut Fossati, Giuliana verfasserin aut Cristina Regondi, Maria verfasserin aut Pattini, Linda verfasserin aut Frassoni, Carolina verfasserin aut Francolini, Maura verfasserin aut Scita, Giorgio verfasserin aut Sala, Mariaelvina verfasserin aut Fahnestock, Margaret verfasserin aut Matteoli, Michela verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 32(2013), 12 vom: 17. Mai, Seite 1730-1744 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:32 year:2013 number:12 day:17 month:05 pages:1730-1744 https://dx.doi.org/10.1038/emboj.2013.107 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 32 2013 12 17 05 1730-1744 |
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10.1038/emboj.2013.107 doi (DE-627)SPR057868689 (SPR)emboj.2013.107-e DE-627 ger DE-627 rakwb eng Menna, Elisabetta verfasserin aut Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2013 Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape and synaptic strength and, consistently, abnormalities in spine number and morphology have been described in a number of neurological disorders. In the present study, we demonstrate that the actin‐regulating protein, Eps8, is recruited to the spine head during chemically induced long‐term potentiation in culture and that inhibition of its actin‐capping activity impairs spine enlargement and plasticity. Accordingly, mice lacking Eps8 display immature spines, which are unable to undergo potentiation, and are impaired in cognitive functions. Additionally, we found that reduction in the levels of Eps8 occurs in brains of patients affected by autism compared to controls. Our data reveal the key role of Eps8 actin‐capping activity in spine morphogenesis and plasticity and indicate that reductions in actin‐capping proteins may characterize forms of intellectual disabilities associated with spine defects. Abstract Reduced Eps8 levels in brains of autism patients correlate with impaired spine morphogenesis and cognitive function in Eps8‐deficient mice, suggesting causal links between actin‐remodelling defects and certain intellectual disabilities. actin‐capping activity (dpeaa)DE-He213 activity‐dependent plasticity (dpeaa)DE-He213 Eps8 (dpeaa)DE-He213 learning and memory defects (dpeaa)DE-He213 spine morphogenesis (dpeaa)DE-He213 Zambetti, Stefania verfasserin aut Morini, Raffaella verfasserin aut Donzelli, Andrea verfasserin aut Disanza, Andrea verfasserin aut Calvigioni, Daniela verfasserin aut Braida, Daniela verfasserin aut Nicolini, Chiara verfasserin aut Orlando, Marta verfasserin aut Fossati, Giuliana verfasserin aut Cristina Regondi, Maria verfasserin aut Pattini, Linda verfasserin aut Frassoni, Carolina verfasserin aut Francolini, Maura verfasserin aut Scita, Giorgio verfasserin aut Sala, Mariaelvina verfasserin aut Fahnestock, Margaret verfasserin aut Matteoli, Michela verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 32(2013), 12 vom: 17. Mai, Seite 1730-1744 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:32 year:2013 number:12 day:17 month:05 pages:1730-1744 https://dx.doi.org/10.1038/emboj.2013.107 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 32 2013 12 17 05 1730-1744 |
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10.1038/emboj.2013.107 doi (DE-627)SPR057868689 (SPR)emboj.2013.107-e DE-627 ger DE-627 rakwb eng Menna, Elisabetta verfasserin aut Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2013 Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape and synaptic strength and, consistently, abnormalities in spine number and morphology have been described in a number of neurological disorders. In the present study, we demonstrate that the actin‐regulating protein, Eps8, is recruited to the spine head during chemically induced long‐term potentiation in culture and that inhibition of its actin‐capping activity impairs spine enlargement and plasticity. Accordingly, mice lacking Eps8 display immature spines, which are unable to undergo potentiation, and are impaired in cognitive functions. Additionally, we found that reduction in the levels of Eps8 occurs in brains of patients affected by autism compared to controls. Our data reveal the key role of Eps8 actin‐capping activity in spine morphogenesis and plasticity and indicate that reductions in actin‐capping proteins may characterize forms of intellectual disabilities associated with spine defects. Abstract Reduced Eps8 levels in brains of autism patients correlate with impaired spine morphogenesis and cognitive function in Eps8‐deficient mice, suggesting causal links between actin‐remodelling defects and certain intellectual disabilities. actin‐capping activity (dpeaa)DE-He213 activity‐dependent plasticity (dpeaa)DE-He213 Eps8 (dpeaa)DE-He213 learning and memory defects (dpeaa)DE-He213 spine morphogenesis (dpeaa)DE-He213 Zambetti, Stefania verfasserin aut Morini, Raffaella verfasserin aut Donzelli, Andrea verfasserin aut Disanza, Andrea verfasserin aut Calvigioni, Daniela verfasserin aut Braida, Daniela verfasserin aut Nicolini, Chiara verfasserin aut Orlando, Marta verfasserin aut Fossati, Giuliana verfasserin aut Cristina Regondi, Maria verfasserin aut Pattini, Linda verfasserin aut Frassoni, Carolina verfasserin aut Francolini, Maura verfasserin aut Scita, Giorgio verfasserin aut Sala, Mariaelvina verfasserin aut Fahnestock, Margaret verfasserin aut Matteoli, Michela verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 32(2013), 12 vom: 17. Mai, Seite 1730-1744 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:32 year:2013 number:12 day:17 month:05 pages:1730-1744 https://dx.doi.org/10.1038/emboj.2013.107 X:SPRINGER Resolving-System lizenzpflichtig Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 32 2013 12 17 05 1730-1744 |
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Menna, Elisabetta @@aut@@ Zambetti, Stefania @@aut@@ Morini, Raffaella @@aut@@ Donzelli, Andrea @@aut@@ Disanza, Andrea @@aut@@ Calvigioni, Daniela @@aut@@ Braida, Daniela @@aut@@ Nicolini, Chiara @@aut@@ Orlando, Marta @@aut@@ Fossati, Giuliana @@aut@@ Cristina Regondi, Maria @@aut@@ Pattini, Linda @@aut@@ Frassoni, Carolina @@aut@@ Francolini, Maura @@aut@@ Scita, Giorgio @@aut@@ Sala, Mariaelvina @@aut@@ Fahnestock, Margaret @@aut@@ Matteoli, Michela @@aut@@ |
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Menna, Elisabetta |
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Menna, Elisabetta misc actin‐capping activity misc activity‐dependent plasticity misc Eps8 misc learning and memory defects misc spine morphogenesis Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity |
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Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity actin‐capping activity (dpeaa)DE-He213 activity‐dependent plasticity (dpeaa)DE-He213 Eps8 (dpeaa)DE-He213 learning and memory defects (dpeaa)DE-He213 spine morphogenesis (dpeaa)DE-He213 |
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misc actin‐capping activity misc activity‐dependent plasticity misc Eps8 misc learning and memory defects misc spine morphogenesis |
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misc actin‐capping activity misc activity‐dependent plasticity misc Eps8 misc learning and memory defects misc spine morphogenesis |
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Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity |
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Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity |
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Menna, Elisabetta |
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Menna, Elisabetta Zambetti, Stefania Morini, Raffaella Donzelli, Andrea Disanza, Andrea Calvigioni, Daniela Braida, Daniela Nicolini, Chiara Orlando, Marta Fossati, Giuliana Cristina Regondi, Maria Pattini, Linda Frassoni, Carolina Francolini, Maura Scita, Giorgio Sala, Mariaelvina Fahnestock, Margaret Matteoli, Michela |
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Elektronische Aufsätze |
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Menna, Elisabetta |
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10.1038/emboj.2013.107 |
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eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity |
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Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity |
| abstract |
Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape and synaptic strength and, consistently, abnormalities in spine number and morphology have been described in a number of neurological disorders. In the present study, we demonstrate that the actin‐regulating protein, Eps8, is recruited to the spine head during chemically induced long‐term potentiation in culture and that inhibition of its actin‐capping activity impairs spine enlargement and plasticity. Accordingly, mice lacking Eps8 display immature spines, which are unable to undergo potentiation, and are impaired in cognitive functions. Additionally, we found that reduction in the levels of Eps8 occurs in brains of patients affected by autism compared to controls. Our data reveal the key role of Eps8 actin‐capping activity in spine morphogenesis and plasticity and indicate that reductions in actin‐capping proteins may characterize forms of intellectual disabilities associated with spine defects. Abstract Reduced Eps8 levels in brains of autism patients correlate with impaired spine morphogenesis and cognitive function in Eps8‐deficient mice, suggesting causal links between actin‐remodelling defects and certain intellectual disabilities. © European Molecular Biology Organization 2013 |
| abstractGer |
Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape and synaptic strength and, consistently, abnormalities in spine number and morphology have been described in a number of neurological disorders. In the present study, we demonstrate that the actin‐regulating protein, Eps8, is recruited to the spine head during chemically induced long‐term potentiation in culture and that inhibition of its actin‐capping activity impairs spine enlargement and plasticity. Accordingly, mice lacking Eps8 display immature spines, which are unable to undergo potentiation, and are impaired in cognitive functions. Additionally, we found that reduction in the levels of Eps8 occurs in brains of patients affected by autism compared to controls. Our data reveal the key role of Eps8 actin‐capping activity in spine morphogenesis and plasticity and indicate that reductions in actin‐capping proteins may characterize forms of intellectual disabilities associated with spine defects. Abstract Reduced Eps8 levels in brains of autism patients correlate with impaired spine morphogenesis and cognitive function in Eps8‐deficient mice, suggesting causal links between actin‐remodelling defects and certain intellectual disabilities. © European Molecular Biology Organization 2013 |
| abstract_unstemmed |
Abstract Actin‐based remodelling underlies spine structural changes occurring during synaptic plasticity, the process that constantly reshapes the circuitry of the adult brain in response to external stimuli, leading to learning and memory formation. A positive correlation exists between spine shape and synaptic strength and, consistently, abnormalities in spine number and morphology have been described in a number of neurological disorders. In the present study, we demonstrate that the actin‐regulating protein, Eps8, is recruited to the spine head during chemically induced long‐term potentiation in culture and that inhibition of its actin‐capping activity impairs spine enlargement and plasticity. Accordingly, mice lacking Eps8 display immature spines, which are unable to undergo potentiation, and are impaired in cognitive functions. Additionally, we found that reduction in the levels of Eps8 occurs in brains of patients affected by autism compared to controls. Our data reveal the key role of Eps8 actin‐capping activity in spine morphogenesis and plasticity and indicate that reductions in actin‐capping proteins may characterize forms of intellectual disabilities associated with spine defects. Abstract Reduced Eps8 levels in brains of autism patients correlate with impaired spine morphogenesis and cognitive function in Eps8‐deficient mice, suggesting causal links between actin‐remodelling defects and certain intellectual disabilities. © European Molecular Biology Organization 2013 |
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Eps8 controls dendritic spine density and synaptic plasticity through its actin‐capping activity |
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Zambetti, Stefania Morini, Raffaella Donzelli, Andrea Disanza, Andrea Calvigioni, Daniela Braida, Daniela Nicolini, Chiara Orlando, Marta Fossati, Giuliana Cristina Regondi, Maria Pattini, Linda Frassoni, Carolina Francolini, Maura Scita, Giorgio Sala, Mariaelvina Fahnestock, Margaret Matteoli, Michela |
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| score |
7.4010124 |