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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)
[article]
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 Ketogenic diet modifies the gut microbiota in a murine model of autism spectrum disorder / C. NEWELL in Molecular Autism, 7 (2016)
[article]
Titre : Ketogenic diet modifies the gut microbiota in a murine model of autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : C. NEWELL, Auteur ; M. R. BOMHOF, Auteur ; R. A. REIMER, Auteur ; D. S. HITTEL, Auteur ; J. M. RHO, Auteur ; J. SHEARER, Auteur Article en page(s) : 37p. Langues : Anglais (eng) Mots-clés : Animals Autism Spectrum Disorder/microbiology Bacteria/isolation & purification Behavior, Animal Cecum/microbiology Diet, Ketogenic Disease Models, Animal Feces/microbiology Gastrointestinal Microbiome Male Mice Mice, Inbred C57BL Social Behavior Autism spectrum disorder BTBR mouse Gut microbiome Ketogenic diet Index. décimale : PER Périodiques Résumé : BACKGROUND: Gastrointestinal dysfunction and gut microbial composition disturbances have been widely reported in autism spectrum disorder (ASD). This study examines whether gut microbiome disturbances are present in the BTBR(T + tf/j) (BTBR) mouse model of ASD and if the ketogenic diet, a diet previously shown to elicit therapeutic benefit in this mouse model, is capable of altering the profile. FINDINGS: Juvenile male C57BL/6 (B6) and BTBR mice were fed a standard chow (CH, 13 % kcal fat) or ketogenic diet (KD, 75 % kcal fat) for 10-14 days. Following diets, fecal and cecal samples were collected for analysis. Main findings are as follows: (1) gut microbiota compositions of cecal and fecal samples were altered in BTBR compared to control mice, indicating that this model may be of utility in understanding gut-brain interactions in ASD; (2) KD consumption caused an anti-microbial-like effect by significantly decreasing total host bacterial abundance in cecal and fecal matter; (3) specific to BTBR animals, the KD counteracted the common ASD phenotype of a low Firmicutes to Bacteroidetes ratio in both sample types; and (4) the KD reversed elevated Akkermansia muciniphila content in the cecal and fecal matter of BTBR animals. CONCLUSIONS: Results indicate that consumption of a KD likely triggers reductions in total gut microbial counts and compositional remodeling in the BTBR mouse. These findings may explain, in part, the ability of a KD to mitigate some of the neurological symptoms associated with ASD in an animal model. En ligne : http://dx.doi.org/10.1186/s13229-016-0099-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328
in Molecular Autism > 7 (2016) . - 37p.[article] Ketogenic diet modifies the gut microbiota in a murine model of autism spectrum disorder [Texte imprimé et/ou numérique] / C. NEWELL, Auteur ; M. R. BOMHOF, Auteur ; R. A. REIMER, Auteur ; D. S. HITTEL, Auteur ; J. M. RHO, Auteur ; J. SHEARER, Auteur . - 37p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 37p.
Mots-clés : Animals Autism Spectrum Disorder/microbiology Bacteria/isolation & purification Behavior, Animal Cecum/microbiology Diet, Ketogenic Disease Models, Animal Feces/microbiology Gastrointestinal Microbiome Male Mice Mice, Inbred C57BL Social Behavior Autism spectrum disorder BTBR mouse Gut microbiome Ketogenic diet Index. décimale : PER Périodiques Résumé : BACKGROUND: Gastrointestinal dysfunction and gut microbial composition disturbances have been widely reported in autism spectrum disorder (ASD). This study examines whether gut microbiome disturbances are present in the BTBR(T + tf/j) (BTBR) mouse model of ASD and if the ketogenic diet, a diet previously shown to elicit therapeutic benefit in this mouse model, is capable of altering the profile. FINDINGS: Juvenile male C57BL/6 (B6) and BTBR mice were fed a standard chow (CH, 13 % kcal fat) or ketogenic diet (KD, 75 % kcal fat) for 10-14 days. Following diets, fecal and cecal samples were collected for analysis. Main findings are as follows: (1) gut microbiota compositions of cecal and fecal samples were altered in BTBR compared to control mice, indicating that this model may be of utility in understanding gut-brain interactions in ASD; (2) KD consumption caused an anti-microbial-like effect by significantly decreasing total host bacterial abundance in cecal and fecal matter; (3) specific to BTBR animals, the KD counteracted the common ASD phenotype of a low Firmicutes to Bacteroidetes ratio in both sample types; and (4) the KD reversed elevated Akkermansia muciniphila content in the cecal and fecal matter of BTBR animals. CONCLUSIONS: Results indicate that consumption of a KD likely triggers reductions in total gut microbial counts and compositional remodeling in the BTBR mouse. These findings may explain, in part, the ability of a KD to mitigate some of the neurological symptoms associated with ASD in an animal model. En ligne : http://dx.doi.org/10.1186/s13229-016-0099-3 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328