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Auteur Maryam KHANBABAEI |
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Disruption of visual circuit formation and refinement in a mouse model of autism / Ning CHENG in Autism Research, 10-2 (February 2017)
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Titre : Disruption of visual circuit formation and refinement in a mouse model of autism Type de document : Texte imprimé et/ou numérique Auteurs : Ning CHENG, Auteur ; Maryam KHANBABAEI, Auteur ; Kartikeya MURARI, Auteur ; Jong M. RHO, Auteur Article en page(s) : p.212-223 Langues : Anglais (eng) Mots-clés : autism spectrum disorder brain circuit synaptic patterning visual system lateral geniculate nucleus eye-specific segregation BTBR mouse Index. décimale : PER Périodiques Résumé : Aberrant connectivity is believed to contribute to the pathophysiology of autism spectrum disorder (ASD). Recent neuroimaging studies have increasingly identified such impairments in patients with ASD, including alterations in sensory systems. However, the cellular substrates and molecular underpinnings of disrupted connectivity remain poorly understood. Utilizing eye-specific segregation in the dorsal lateral geniculate nucleus (dLGN) as a model system, we investigated the formation and refinement of precise patterning of synaptic connections in the BTBR T?+?tf/J (BTBR) mouse model of ASD. We found that at the neonatal stage, the shape of the dLGN occupied by retinal afferents was altered in the BTBR group compared to C57BL/6J (B6) animals. Notably, the degree of overlap between the ipsi- and contralateral afferents was significantly greater in the BTBR mice. Moreover, these abnormalities continued into mature stage in the BTBR animals, suggesting persistent deficits rather than delayed maturation of axonal refinement. Together, these results indicate disrupted connectivity at the synaptic patterning level in the BTBR mice, suggesting that in general, altered neural circuitry may contribute to autistic behaviours seen in this animal model. In addition, these data are consistent with the notion that lower-level, primary processing mechanisms contribute to altered visual perception in ASD. En ligne : http://dx.doi.org/10.1002/aur.1687 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=303
in Autism Research > 10-2 (February 2017) . - p.212-223[article] Disruption of visual circuit formation and refinement in a mouse model of autism [Texte imprimé et/ou numérique] / Ning CHENG, Auteur ; Maryam KHANBABAEI, Auteur ; Kartikeya MURARI, Auteur ; Jong M. RHO, Auteur . - p.212-223.
Langues : Anglais (eng)
in Autism Research > 10-2 (February 2017) . - p.212-223
Mots-clés : autism spectrum disorder brain circuit synaptic patterning visual system lateral geniculate nucleus eye-specific segregation BTBR mouse Index. décimale : PER Périodiques Résumé : Aberrant connectivity is believed to contribute to the pathophysiology of autism spectrum disorder (ASD). Recent neuroimaging studies have increasingly identified such impairments in patients with ASD, including alterations in sensory systems. However, the cellular substrates and molecular underpinnings of disrupted connectivity remain poorly understood. Utilizing eye-specific segregation in the dorsal lateral geniculate nucleus (dLGN) as a model system, we investigated the formation and refinement of precise patterning of synaptic connections in the BTBR T?+?tf/J (BTBR) mouse model of ASD. We found that at the neonatal stage, the shape of the dLGN occupied by retinal afferents was altered in the BTBR group compared to C57BL/6J (B6) animals. Notably, the degree of overlap between the ipsi- and contralateral afferents was significantly greater in the BTBR mice. Moreover, these abnormalities continued into mature stage in the BTBR animals, suggesting persistent deficits rather than delayed maturation of axonal refinement. Together, these results indicate disrupted connectivity at the synaptic patterning level in the BTBR mice, suggesting that in general, altered neural circuitry may contribute to autistic behaviours seen in this animal model. In addition, these data are consistent with the notion that lower-level, primary processing mechanisms contribute to altered visual perception in ASD. En ligne : http://dx.doi.org/10.1002/aur.1687 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=303