Abnormal neuronal morphology and altered synaptic proteins are restored by oxytocin in autism-related SHANK3 deficient model
Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are st...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Reichova, Alexandra [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2020transfer abstract |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Serum CCL2 and serum TNF-α – Two new biomarkers predict bone invasion, post-treatment distant metastasis and poor overall survival in nasopharyngeal carcinoma - 2011, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:518 ; year:2020 ; day:1 ; month:12 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1016/j.mce.2020.110924 |
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ELV051876329 |
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| 245 | 1 | 0 | |a Abnormal neuronal morphology and altered synaptic proteins are restored by oxytocin in autism-related SHANK3 deficient model |
| 264 | 1 | |c 2020transfer abstract | |
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| 520 | |a Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. | ||
| 520 | |a Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. | ||
| 650 | 7 | |a Autism |2 Elsevier | |
| 650 | 7 | |a Oxytocin |2 Elsevier | |
| 650 | 7 | |a Neuroligins |2 Elsevier | |
| 650 | 7 | |a Development |2 Elsevier | |
| 650 | 7 | |a SHANK3 |2 Elsevier | |
| 650 | 7 | |a Neurexins |2 Elsevier | |
| 700 | 1 | |a Bacova, Zuzana |4 oth | |
| 700 | 1 | |a Bukatova, Stanislava |4 oth | |
| 700 | 1 | |a Kokavcova, Martina |4 oth | |
| 700 | 1 | |a Meliskova, Veronika |4 oth | |
| 700 | 1 | |a Frimmel, Karel |4 oth | |
| 700 | 1 | |a Ostatnikova, Daniela |4 oth | |
| 700 | 1 | |a Bakos, Jan |4 oth | |
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10.1016/j.mce.2020.110924 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001627.pica (DE-627)ELV051876329 (ELSEVIER)S0303-7207(20)30224-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.52 bkl Reichova, Alexandra verfasserin aut Abnormal neuronal morphology and altered synaptic proteins are restored by oxytocin in autism-related SHANK3 deficient model 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Autism Elsevier Oxytocin Elsevier Neuroligins Elsevier Development Elsevier SHANK3 Elsevier Neurexins Elsevier Bacova, Zuzana oth Bukatova, Stanislava oth Kokavcova, Martina oth Meliskova, Veronika oth Frimmel, Karel oth Ostatnikova, Daniela oth Bakos, Jan oth Enthalten in Elsevier Science Serum CCL2 and serum TNF-α – Two new biomarkers predict bone invasion, post-treatment distant metastasis and poor overall survival in nasopharyngeal carcinoma 2011 Amsterdam [u.a.] (DE-627)ELV010855734 volume:518 year:2020 day:1 month:12 pages:0 https://doi.org/10.1016/j.mce.2020.110924 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.52 Therapie Medizin VZ AR 518 2020 1 1201 0 |
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10.1016/j.mce.2020.110924 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001627.pica (DE-627)ELV051876329 (ELSEVIER)S0303-7207(20)30224-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.52 bkl Reichova, Alexandra verfasserin aut Abnormal neuronal morphology and altered synaptic proteins are restored by oxytocin in autism-related SHANK3 deficient model 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Autism Elsevier Oxytocin Elsevier Neuroligins Elsevier Development Elsevier SHANK3 Elsevier Neurexins Elsevier Bacova, Zuzana oth Bukatova, Stanislava oth Kokavcova, Martina oth Meliskova, Veronika oth Frimmel, Karel oth Ostatnikova, Daniela oth Bakos, Jan oth Enthalten in Elsevier Science Serum CCL2 and serum TNF-α – Two new biomarkers predict bone invasion, post-treatment distant metastasis and poor overall survival in nasopharyngeal carcinoma 2011 Amsterdam [u.a.] (DE-627)ELV010855734 volume:518 year:2020 day:1 month:12 pages:0 https://doi.org/10.1016/j.mce.2020.110924 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.52 Therapie Medizin VZ AR 518 2020 1 1201 0 |
| allfields_unstemmed |
10.1016/j.mce.2020.110924 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001627.pica (DE-627)ELV051876329 (ELSEVIER)S0303-7207(20)30224-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.52 bkl Reichova, Alexandra verfasserin aut Abnormal neuronal morphology and altered synaptic proteins are restored by oxytocin in autism-related SHANK3 deficient model 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Autism Elsevier Oxytocin Elsevier Neuroligins Elsevier Development Elsevier SHANK3 Elsevier Neurexins Elsevier Bacova, Zuzana oth Bukatova, Stanislava oth Kokavcova, Martina oth Meliskova, Veronika oth Frimmel, Karel oth Ostatnikova, Daniela oth Bakos, Jan oth Enthalten in Elsevier Science Serum CCL2 and serum TNF-α – Two new biomarkers predict bone invasion, post-treatment distant metastasis and poor overall survival in nasopharyngeal carcinoma 2011 Amsterdam [u.a.] (DE-627)ELV010855734 volume:518 year:2020 day:1 month:12 pages:0 https://doi.org/10.1016/j.mce.2020.110924 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.52 Therapie Medizin VZ AR 518 2020 1 1201 0 |
| allfieldsGer |
10.1016/j.mce.2020.110924 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001627.pica (DE-627)ELV051876329 (ELSEVIER)S0303-7207(20)30224-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.52 bkl Reichova, Alexandra verfasserin aut Abnormal neuronal morphology and altered synaptic proteins are restored by oxytocin in autism-related SHANK3 deficient model 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Autism Elsevier Oxytocin Elsevier Neuroligins Elsevier Development Elsevier SHANK3 Elsevier Neurexins Elsevier Bacova, Zuzana oth Bukatova, Stanislava oth Kokavcova, Martina oth Meliskova, Veronika oth Frimmel, Karel oth Ostatnikova, Daniela oth Bakos, Jan oth Enthalten in Elsevier Science Serum CCL2 and serum TNF-α – Two new biomarkers predict bone invasion, post-treatment distant metastasis and poor overall survival in nasopharyngeal carcinoma 2011 Amsterdam [u.a.] (DE-627)ELV010855734 volume:518 year:2020 day:1 month:12 pages:0 https://doi.org/10.1016/j.mce.2020.110924 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.52 Therapie Medizin VZ AR 518 2020 1 1201 0 |
| allfieldsSound |
10.1016/j.mce.2020.110924 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001627.pica (DE-627)ELV051876329 (ELSEVIER)S0303-7207(20)30224-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.52 bkl Reichova, Alexandra verfasserin aut Abnormal neuronal morphology and altered synaptic proteins are restored by oxytocin in autism-related SHANK3 deficient model 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. Autism Elsevier Oxytocin Elsevier Neuroligins Elsevier Development Elsevier SHANK3 Elsevier Neurexins Elsevier Bacova, Zuzana oth Bukatova, Stanislava oth Kokavcova, Martina oth Meliskova, Veronika oth Frimmel, Karel oth Ostatnikova, Daniela oth Bakos, Jan oth Enthalten in Elsevier Science Serum CCL2 and serum TNF-α – Two new biomarkers predict bone invasion, post-treatment distant metastasis and poor overall survival in nasopharyngeal carcinoma 2011 Amsterdam [u.a.] (DE-627)ELV010855734 volume:518 year:2020 day:1 month:12 pages:0 https://doi.org/10.1016/j.mce.2020.110924 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 44.52 Therapie Medizin VZ AR 518 2020 1 1201 0 |
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Enthalten in Serum CCL2 and serum TNF-α – Two new biomarkers predict bone invasion, post-treatment distant metastasis and poor overall survival in nasopharyngeal carcinoma Amsterdam [u.a.] volume:518 year:2020 day:1 month:12 pages:0 |
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Enthalten in Serum CCL2 and serum TNF-α – Two new biomarkers predict bone invasion, post-treatment distant metastasis and poor overall survival in nasopharyngeal carcinoma Amsterdam [u.a.] volume:518 year:2020 day:1 month:12 pages:0 |
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Serum CCL2 and serum TNF-α – Two new biomarkers predict bone invasion, post-treatment distant metastasis and poor overall survival in nasopharyngeal carcinoma |
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abnormal neuronal morphology and altered synaptic proteins are restored by oxytocin in autism-related shank3 deficient model |
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Abnormal neuronal morphology and altered synaptic proteins are restored by oxytocin in autism-related SHANK3 deficient model |
| abstract |
Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. |
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Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. |
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Oxytocin has been suggested as a potential therapeutic agent in autism and other neuropsychiatric conditions. Although, the link between the deficit in “SH3 domain and ankyrin repeat containing protein 3” (SHANK3) and autism spectrum disorders is highly studied topic, developmental mechanisms are still poorly understood. In this study, we clearly confirm that SHANK3 deficiency is accompanied with abnormalities in neurite number and length, which are reversed by oxytocin treatment (1 μM, 48h) in primary hippocampal neurons. Transient silencing for the SHANK3 gene (siSHANK3) in neuron-like cell line (SH-SY5Y) revealed a significant decrease in the expression levels of Neurexins 1α, 1β, 2α and 2β. Oxytocin treatment compensated reduced levels of Synapsin I, PSD95 and Neuroligin 3 in siSHANK3 cells suggesting a marked potential of oxytocin to ameliorate defects present in conditions of SHANK3 deficiency. Further analysis of hippocampal tissue revealed that oxytocin application (0.1 μg/μl, s.c. at P2 and P3 day) affects levels of synaptic proteins and GTPases in both WT and SHANK3 deficient mice on day P5. Oxytocin stimulated the mRNA expression of RhoB and Rac1 in both WT and SHANK3 deficient mice. Our data suggest that autism relevant synaptic pathologies could be reversed by oxytocin treatment. |
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