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Exploring the mechanisms underlying excitation/inhibition imbalance in human iPSC-derived models of ASD / Lorenza CULOTTA in Molecular Autism, 11 (2020)
[article]
Titre : Exploring the mechanisms underlying excitation/inhibition imbalance in human iPSC-derived models of ASD Type de document : Texte imprimé et/ou numérique Auteurs : Lorenza CULOTTA, Auteur ; Peter PENZES, Auteur Article en page(s) : 32 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Excitation/inhibition balance Induced pluripotent stem cell Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a range of neurodevelopmental disorders characterized by impaired social interaction and communication, and repetitive or restricted behaviors. ASD subjects exhibit complex genetic and clinical heterogeneity, thus hindering the discovery of pathophysiological mechanisms. Considering that several ASD-risk genes encode proteins involved in the regulation of synaptic plasticity, neuronal excitability, and neuronal connectivity, one hypothesis that has emerged is that ASD arises from a disruption of the neuronal network activity due to perturbation of the synaptic excitation and inhibition (E/I) balance. The development of induced pluripotent stem cell (iPSC) technology and recent advances in neuronal differentiation techniques provide a unique opportunity to model complex neuronal connectivity and to test the E/I hypothesis of ASD in human-based models. Here, we aim to review the latest advances in studying the different cellular and molecular mechanisms contributing to E/I balance using iPSC-based in vitro models of ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00339-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427
in Molecular Autism > 11 (2020) . - 32 p.[article] Exploring the mechanisms underlying excitation/inhibition imbalance in human iPSC-derived models of ASD [Texte imprimé et/ou numérique] / Lorenza CULOTTA, Auteur ; Peter PENZES, Auteur . - 32 p.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020) . - 32 p.
Mots-clés : Autism spectrum disorder Excitation/inhibition balance Induced pluripotent stem cell Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a range of neurodevelopmental disorders characterized by impaired social interaction and communication, and repetitive or restricted behaviors. ASD subjects exhibit complex genetic and clinical heterogeneity, thus hindering the discovery of pathophysiological mechanisms. Considering that several ASD-risk genes encode proteins involved in the regulation of synaptic plasticity, neuronal excitability, and neuronal connectivity, one hypothesis that has emerged is that ASD arises from a disruption of the neuronal network activity due to perturbation of the synaptic excitation and inhibition (E/I) balance. The development of induced pluripotent stem cell (iPSC) technology and recent advances in neuronal differentiation techniques provide a unique opportunity to model complex neuronal connectivity and to test the E/I hypothesis of ASD in human-based models. Here, we aim to review the latest advances in studying the different cellular and molecular mechanisms contributing to E/I balance using iPSC-based in vitro models of ASD. En ligne : http://dx.doi.org/10.1186/s13229-020-00339-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427 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