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17-beta estradiol increases parvalbumin levels in Pvalb heterozygous mice and attenuates behavioral phenotypes with relevance to autism core symptoms / F. FILICE in Molecular Autism, 9 (2018)
[article]
Titre : 17-beta estradiol increases parvalbumin levels in Pvalb heterozygous mice and attenuates behavioral phenotypes with relevance to autism core symptoms Type de document : Texte imprimé et/ou numérique Auteurs : F. FILICE, Auteur ; E. LAUBER, Auteur ; K. J. VORCKEL, Auteur ; M. WOHR, Auteur ; B. SCHWALLER, Auteur Article en page(s) : 15p. Langues : Anglais (eng) Mots-clés : 17-beta estradiol Asd Estradiol treatment Excitation/inhibition balance Parvalbumin Social behavior Ultrasonic vocalizations Index. décimale : PER Périodiques Résumé : Background: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by two core symptoms: impaired social interaction and communication, and restricted, repetitive behaviors and interests. The pathophysiology of ASD is not yet fully understood, due to a plethora of genetic and environmental risk factors that might be associated with or causal for ASD. Recent findings suggest that one putative convergent pathway for some forms of ASD might be the downregulation of the calcium-binding protein parvalbumin (PV). PV-deficient mice (PV-/-, PV+/-), as well as Shank1-/-, Shank3-/-, and VPA mice, which show behavioral deficits relevant to all human ASD core symptoms, are all characterized by lower PV expression levels. Methods: Based on the hypothesis that PV expression might be increased by 17-beta estradiol (E2), PV+/- mice were treated with E2 from postnatal days 5-15 and ASD-related behavior was tested between postnatal days 25 and 31. Results: PV expression levels were significantly increased after E2 treatment and, concomitantly, sociability deficits in PV+/- mice in the direct reciprocal social interaction and the 3-chamber social approach assay, as well as repetitive behaviors, were attenuated. E2 treatment of PV+/+ mice did not increase PV levels and had detrimental effects on sociability and repetitive behavior. In PV-/- mice, E2 obviously did not affect PV levels; tested behaviors were not different from the ones in vehicle-treated PV-/- mice. Conclusion: Our results suggest that the E2-linked amelioration of ASD-like behaviors is specifically occurring in PV+/- mice, indicating that PV upregulation is required for the E2-mediated rescue of ASD-relevant behavioral impairments. En ligne : http://dx.doi.org/10.1186/s13229-018-0199-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=354
in Molecular Autism > 9 (2018) . - 15p.[article] 17-beta estradiol increases parvalbumin levels in Pvalb heterozygous mice and attenuates behavioral phenotypes with relevance to autism core symptoms [Texte imprimé et/ou numérique] / F. FILICE, Auteur ; E. LAUBER, Auteur ; K. J. VORCKEL, Auteur ; M. WOHR, Auteur ; B. SCHWALLER, Auteur . - 15p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 15p.
Mots-clés : 17-beta estradiol Asd Estradiol treatment Excitation/inhibition balance Parvalbumin Social behavior Ultrasonic vocalizations Index. décimale : PER Périodiques Résumé : Background: Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by two core symptoms: impaired social interaction and communication, and restricted, repetitive behaviors and interests. The pathophysiology of ASD is not yet fully understood, due to a plethora of genetic and environmental risk factors that might be associated with or causal for ASD. Recent findings suggest that one putative convergent pathway for some forms of ASD might be the downregulation of the calcium-binding protein parvalbumin (PV). PV-deficient mice (PV-/-, PV+/-), as well as Shank1-/-, Shank3-/-, and VPA mice, which show behavioral deficits relevant to all human ASD core symptoms, are all characterized by lower PV expression levels. Methods: Based on the hypothesis that PV expression might be increased by 17-beta estradiol (E2), PV+/- mice were treated with E2 from postnatal days 5-15 and ASD-related behavior was tested between postnatal days 25 and 31. Results: PV expression levels were significantly increased after E2 treatment and, concomitantly, sociability deficits in PV+/- mice in the direct reciprocal social interaction and the 3-chamber social approach assay, as well as repetitive behaviors, were attenuated. E2 treatment of PV+/+ mice did not increase PV levels and had detrimental effects on sociability and repetitive behavior. In PV-/- mice, E2 obviously did not affect PV levels; tested behaviors were not different from the ones in vehicle-treated PV-/- mice. Conclusion: Our results suggest that the E2-linked amelioration of ASD-like behaviors is specifically occurring in PV+/- mice, indicating that PV upregulation is required for the E2-mediated rescue of ASD-relevant behavioral impairments. En ligne : http://dx.doi.org/10.1186/s13229-018-0199-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=354 Age-specific autistic-like behaviors in heterozygous Fmr1-KO female mice / Manon GAUDUCHEAU in Autism Research, 10-6 (June 2017)
[article]
Titre : Age-specific autistic-like behaviors in heterozygous Fmr1-KO female mice Type de document : Texte imprimé et/ou numérique Auteurs : Manon GAUDUCHEAU, Auteur ; Valerie LEMAIRE-MAYO, Auteur ; Francesca R. D'AMATO, Auteur ; Diego ODDI, Auteur ; Wim E. CRUSIO, Auteur ; Susanna PIETROPAOLO, Auteur Article en page(s) : p.1067-1078 Langues : Anglais (eng) Mots-clés : adolescence ultrasonic vocalizations social interactions developmental disorders Fragile X syndrome animal models autism Index. décimale : PER Périodiques Résumé : Fragile X syndrome (FXS) is a major developmental disorder and the most frequent monogenic cause of autism. Surprisingly, most existing studies on the Fmr1-KO mouse model for FXS have focused on males, although FX women, who are mostly heterozygous for the Fmr1 mutation, are known to exhibit several behavioral deficits, including autistic-like features. Furthermore, most animal research has been carried out on adults only; so that little is known about the age progression of the behavioral phenotype of Fmr1 mutants, which is a crucial issue to optimize the impact of therapeutic interventions. Here, we performed an extensive analysis of autistic-like social behaviors in heterozygous (HET) Fmr1-KO females and their WT littermates at different ages. No behavioral difference between HET and WT mice was observed at infancy, but some abnormalities in social interaction and communication were first detected at juvenile age. At adulthood some of these alterations disappeared, but avoidance of social novelty appeared, together with other FXS-relevant behavioral deficits, such as hyperactivity and reduced contextual fear response. Our data provide for the first time evidence for the presence of autistic-relevant behavioral abnormalities in Fmr1-HET female mice, demonstrating the utility of this mouse line to model autistic-like behaviors in both sexes. These results also highlight the importance of taking into account age differences when using the Fmr1-KO mouse model, suggesting that the early post-natal phases are the most promising target for preventive interventions and the adult age is the most appropriate to investigate the behavioral impact of potential therapies. En ligne : http://dx.doi.org/10.1002/aur.1743 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=309
in Autism Research > 10-6 (June 2017) . - p.1067-1078[article] Age-specific autistic-like behaviors in heterozygous Fmr1-KO female mice [Texte imprimé et/ou numérique] / Manon GAUDUCHEAU, Auteur ; Valerie LEMAIRE-MAYO, Auteur ; Francesca R. D'AMATO, Auteur ; Diego ODDI, Auteur ; Wim E. CRUSIO, Auteur ; Susanna PIETROPAOLO, Auteur . - p.1067-1078.
Langues : Anglais (eng)
in Autism Research > 10-6 (June 2017) . - p.1067-1078
Mots-clés : adolescence ultrasonic vocalizations social interactions developmental disorders Fragile X syndrome animal models autism Index. décimale : PER Périodiques Résumé : Fragile X syndrome (FXS) is a major developmental disorder and the most frequent monogenic cause of autism. Surprisingly, most existing studies on the Fmr1-KO mouse model for FXS have focused on males, although FX women, who are mostly heterozygous for the Fmr1 mutation, are known to exhibit several behavioral deficits, including autistic-like features. Furthermore, most animal research has been carried out on adults only; so that little is known about the age progression of the behavioral phenotype of Fmr1 mutants, which is a crucial issue to optimize the impact of therapeutic interventions. Here, we performed an extensive analysis of autistic-like social behaviors in heterozygous (HET) Fmr1-KO females and their WT littermates at different ages. No behavioral difference between HET and WT mice was observed at infancy, but some abnormalities in social interaction and communication were first detected at juvenile age. At adulthood some of these alterations disappeared, but avoidance of social novelty appeared, together with other FXS-relevant behavioral deficits, such as hyperactivity and reduced contextual fear response. Our data provide for the first time evidence for the presence of autistic-relevant behavioral abnormalities in Fmr1-HET female mice, demonstrating the utility of this mouse line to model autistic-like behaviors in both sexes. These results also highlight the importance of taking into account age differences when using the Fmr1-KO mouse model, suggesting that the early post-natal phases are the most promising target for preventive interventions and the adult age is the most appropriate to investigate the behavioral impact of potential therapies. En ligne : http://dx.doi.org/10.1002/aur.1743 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=309 Serotonin Disturbance in Mouse Models of Autism Spectrum Disorders / Kota TAMADA
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