Absence of preference for social novelty and increased grooming in integrin β3 knockout mice: Initial studies and future directions / Michelle D. CARTER in Autism Research, 4-1 (February 2011)  

Public ISBD [article]  inAutism Research > 4-1 (February 2011) . - p.57-67 Titre : Absence of preference for social novelty and increased grooming in integrin β3 knockout mice: Initial studies and future directions Type de document : texte imprimé Auteurs : Michelle D. CARTER, Auteur ; Charisma R. SHAH, Auteur ; Christopher L. MULLER, Auteur ; Jacqueline N. CRAWLEY, Auteur ; Ana M.D. CARNEIRO, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur Année de publication : 2011 Article en page(s) : p.57-67 Langues : Anglais (eng) Mots-clés : autism  genetic  integrin  cell adhesion  serotonin  social memory  grooming  obsessive–compulsive disorder Index. décimale : PER Périodiques Résumé : Elevated whole blood serotonin 5-HT, or hyperserotonemia, is a common biomarker in autism spectrum disorder (ASD). The integrin β3 receptor subunit gene (ITGB3) is a quantitative trait locus for whole blood 5-HT levels. Recent work shows that integrin β3 interacts with the serotonin transporter (SERT) in both platelets and in the midbrain. Furthermore, multiple studies have now reported gene–gene interaction between the integrin β3 and SERT genes in association with ASD. Given the lack of previous data on the impact of integrin β3 on brain or behavioral phenotypes, we sought to compare mice with decreased or absent expression of the integrin β3 receptor subunit (Itgb3 + / − and −/ −) with wildtype littermate controls in behavioral tasks relevant to ASD. These mice did not show deficits in activity level in the open field or anxiety-like behavior on the elevated plus maze, two potential confounds in the evaluation of mouse social behavior. In the three-chamber social test, mice lacking integrin β3 were shown to have normal sociability but did not show a preference for social novelty. Importantly, the absence of integrin β3 did not impair olfaction or the ability to recall familiar social odors. Additionally, mice lacking integrin β3 showed increased grooming behavior in novel environments. These preliminary studies reveal altered social and repetitive behavior in these mice, which suggests that the integrin β3 subunit may be involved in brain systems relevant to ASD. Further work is needed to fully characterize these behavioral changes and the underlying brain mechanisms. En ligne : http://dx.doi.org/10.1002/aur.180 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=118 [article] Absence of preference for social novelty and increased grooming in integrin β3 knockout mice: Initial studies and future directions [texte imprimé] / Michelle D. CARTER, Auteur ; Charisma R. SHAH, Auteur ; Christopher L. MULLER, Auteur ; Jacqueline N. CRAWLEY, Auteur ; Ana M.D. CARNEIRO, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur . - 2011 . - p.57-67. Langues : Anglais (eng) in Autism Research > 4-1 (February 2011) . - p.57-67 Mots-clés : autism  genetic  integrin  cell adhesion  serotonin  social memory  grooming  obsessive–compulsive disorder Index. décimale : PER Périodiques Résumé : Elevated whole blood serotonin 5-HT, or hyperserotonemia, is a common biomarker in autism spectrum disorder (ASD). The integrin β3 receptor subunit gene (ITGB3) is a quantitative trait locus for whole blood 5-HT levels. Recent work shows that integrin β3 interacts with the serotonin transporter (SERT) in both platelets and in the midbrain. Furthermore, multiple studies have now reported gene–gene interaction between the integrin β3 and SERT genes in association with ASD. Given the lack of previous data on the impact of integrin β3 on brain or behavioral phenotypes, we sought to compare mice with decreased or absent expression of the integrin β3 receptor subunit (Itgb3 + / − and −/ −) with wildtype littermate controls in behavioral tasks relevant to ASD. These mice did not show deficits in activity level in the open field or anxiety-like behavior on the elevated plus maze, two potential confounds in the evaluation of mouse social behavior. In the three-chamber social test, mice lacking integrin β3 were shown to have normal sociability but did not show a preference for social novelty. Importantly, the absence of integrin β3 did not impair olfaction or the ability to recall familiar social odors. Additionally, mice lacking integrin β3 showed increased grooming behavior in novel environments. These preliminary studies reveal altered social and repetitive behavior in these mice, which suggests that the integrin β3 subunit may be involved in brain systems relevant to ASD. Further work is needed to fully characterize these behavioral changes and the underlying brain mechanisms. En ligne : http://dx.doi.org/10.1002/aur.180 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=118

Genetic background modulates phenotypes of serotonin transporter Ala56 knock-in mice / Travis KERR in Molecular Autism, (October 2013)  

Public ISBD [article]  inMolecular Autism > (October 2013) Titre : Genetic background modulates phenotypes of serotonin transporter Ala56 knock-in mice Type de document : texte imprimé Auteurs : Travis KERR, Auteur ; Christopher L. MULLER, Auteur ; Mahfuzur MIAH, Auteur ; Christopher JETTER, Auteur ; Rita PFEIFFER, Auteur ; Charisma SHAH, Auteur ; Nicole BAGANZ, Auteur ; George M. ANDERSON, Auteur ; Jacqueline N. CRAWLEY, Auteur ; James SUTCLIFFE, Auteur ; Randy BLAKELY, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Previously, we identified multiple, rare serotonin (5-HT) transporter (SERT) variants in children with autism spectrum disorder (ASD). Although in our study the SERT Ala56 variant was over-transmitted to ASD probands, it was also seen in some unaffected individuals, suggesting that associated ASD risk is influenced by the epistatic effects of other genetic variation. Subsequently, we established that mice expressing the SERT Ala56 variant on a 129S6/S4 genetic background display multiple biochemical, physiological and behavioral changes, including hyperserotonemia, altered 5-HT receptor sensitivity, and altered social, communication, and repetitive behavior. Here we explore the effects of genetic background on SERT Ala56 knock-in phenotypes. To explore the effects of genetic background, we backcrossed SERT Ala56 mice on the 129 background into a C57BL/6 (B6) background to achieve congenic B6 SERT Ala56 mice, and assessed autism-relevant behavior, including sociability, ultrasonic vocalizations, and repetitive behavior in the home cage, as well as serotonergic phenotypes, including whole blood serotonin levels and serotonin receptor sensitivity. One consistent phenotype between the two strains was performance in the tube test for dominance, where mutant mice displayed a greater tendency to withdraw from a social encounter in a narrow tube as compared to wildtype littermate controls. On the B6 background, mutant pup ultrasonic vocalizations were significantly increased, in contrast to decreased vocalizations seen previously on the 129 background. Several phenotypes seen on the 129 background were reduced or absent when the mutation was placed on the B6 background, including hyperserotonemia, 5-HT receptor hypersensivity, and repetitive behavior. Our findings provide a cogent example of how epistatic interactions can modulate the impact of functional genetic variation and suggest that some aspects of social behavior may be especially sensitive to changes in SERT function. Finally, these results provide a platform for the identification of genes that may modulate the risk of ASD in humans. En ligne : http://dx.doi.org/10.1186/2040-2392-4-35 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227 [article] Genetic background modulates phenotypes of serotonin transporter Ala56 knock-in mice [texte imprimé] / Travis KERR, Auteur ; Christopher L. MULLER, Auteur ; Mahfuzur MIAH, Auteur ; Christopher JETTER, Auteur ; Rita PFEIFFER, Auteur ; Charisma SHAH, Auteur ; Nicole BAGANZ, Auteur ; George M. ANDERSON, Auteur ; Jacqueline N. CRAWLEY, Auteur ; James SUTCLIFFE, Auteur ; Randy BLAKELY, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur. Langues : Anglais (eng) in Molecular Autism > (October 2013) Index. décimale : PER Périodiques Résumé : Previously, we identified multiple, rare serotonin (5-HT) transporter (SERT) variants in children with autism spectrum disorder (ASD). Although in our study the SERT Ala56 variant was over-transmitted to ASD probands, it was also seen in some unaffected individuals, suggesting that associated ASD risk is influenced by the epistatic effects of other genetic variation. Subsequently, we established that mice expressing the SERT Ala56 variant on a 129S6/S4 genetic background display multiple biochemical, physiological and behavioral changes, including hyperserotonemia, altered 5-HT receptor sensitivity, and altered social, communication, and repetitive behavior. Here we explore the effects of genetic background on SERT Ala56 knock-in phenotypes. To explore the effects of genetic background, we backcrossed SERT Ala56 mice on the 129 background into a C57BL/6 (B6) background to achieve congenic B6 SERT Ala56 mice, and assessed autism-relevant behavior, including sociability, ultrasonic vocalizations, and repetitive behavior in the home cage, as well as serotonergic phenotypes, including whole blood serotonin levels and serotonin receptor sensitivity. One consistent phenotype between the two strains was performance in the tube test for dominance, where mutant mice displayed a greater tendency to withdraw from a social encounter in a narrow tube as compared to wildtype littermate controls. On the B6 background, mutant pup ultrasonic vocalizations were significantly increased, in contrast to decreased vocalizations seen previously on the 129 background. Several phenotypes seen on the 129 background were reduced or absent when the mutation was placed on the B6 background, including hyperserotonemia, 5-HT receptor hypersensivity, and repetitive behavior. Our findings provide a cogent example of how epistatic interactions can modulate the impact of functional genetic variation and suggest that some aspects of social behavior may be especially sensitive to changes in SERT function. Finally, these results provide a platform for the identification of genes that may modulate the risk of ASD in humans. En ligne : http://dx.doi.org/10.1186/2040-2392-4-35 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=227

Letting a Typical Mouse Judge Whether Mouse Social Interactions Are Atypical / Charisma R. SHAH in Autism Research, 6-3 (June 2013)  

Public ISBD [article]  inAutism Research > 6-3 (June 2013) . - p.212-220 Titre : Letting a Typical Mouse Judge Whether Mouse Social Interactions Are Atypical Type de document : texte imprimé Auteurs : Charisma R. SHAH, Auteur ; Carl Gunnar FORSBERG, Auteur ; Jing-Qiong KANG, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur Année de publication : 2013 Article en page(s) : p.212-220 Langues : Anglais (eng) Mots-clés : animal models  behavioral analysis of animal models??animal models  genetics  gamma-aminobutyric acid neurochemistry Index. décimale : PER Périodiques Résumé : Diagnosis of an autism spectrum disorder (ASD) requires a qualitative assessment of social aptitude: one person judging whether another person interacts in a “typical” way. We hypothesized that mice could be used to make a similar judgment if they prefer “typical” over “atypical” social interactions with mouse models relevant to ASD. We used wild-type C57BL/6 (B6) mice as “judges” and evaluated their preference for a chamber containing a “typical” (B6 or 129S6) or an “atypical” mouse. For our atypical mouse stimuli, we chose two inbred strains with well-documented social phenotypes (BTBR and BALB/c), as well a mutant line with abnormal social behavior and seizures (Gabrb3 +/−). Overall, we observed a stimulus by time interaction (P  0.0001), with B6 mice preferring the typical mouse chamber during the last 10 min of the 30-min test. For two of the individual stimulus pairings, we observed a similar chamber by time interaction (BALB/c vs. 129S6, P = 0.0007; Gabrb3 +/− vs. 129S6, P = 0.033). For the third stimulus pairing, we found a trend for preference of the typical mouse across time (BTBR vs. B6, P = 0.051). We repeated the experiments using 129S6 mice as judges and found a significant overall interaction (P = 0.034), but only one stimulus pairing reached significance on its own (BALB/c vs. 129S6, P = 0.0021). These data suggest that a characteristic pattern of exploration in B6 mice can distinguish some socially atypical animals from controls. En ligne : http://dx.doi.org/10.1002/aur.1280 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202 [article] Letting a Typical Mouse Judge Whether Mouse Social Interactions Are Atypical [texte imprimé] / Charisma R. SHAH, Auteur ; Carl Gunnar FORSBERG, Auteur ; Jing-Qiong KANG, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur . - 2013 . - p.212-220. Langues : Anglais (eng) in Autism Research > 6-3 (June 2013) . - p.212-220 Mots-clés : animal models  behavioral analysis of animal models??animal models  genetics  gamma-aminobutyric acid neurochemistry Index. décimale : PER Périodiques Résumé : Diagnosis of an autism spectrum disorder (ASD) requires a qualitative assessment of social aptitude: one person judging whether another person interacts in a “typical” way. We hypothesized that mice could be used to make a similar judgment if they prefer “typical” over “atypical” social interactions with mouse models relevant to ASD. We used wild-type C57BL/6 (B6) mice as “judges” and evaluated their preference for a chamber containing a “typical” (B6 or 129S6) or an “atypical” mouse. For our atypical mouse stimuli, we chose two inbred strains with well-documented social phenotypes (BTBR and BALB/c), as well a mutant line with abnormal social behavior and seizures (Gabrb3 +/−). Overall, we observed a stimulus by time interaction (P  0.0001), with B6 mice preferring the typical mouse chamber during the last 10 min of the 30-min test. For two of the individual stimulus pairings, we observed a similar chamber by time interaction (BALB/c vs. 129S6, P = 0.0007; Gabrb3 +/− vs. 129S6, P = 0.033). For the third stimulus pairing, we found a trend for preference of the typical mouse across time (BTBR vs. B6, P = 0.051). We repeated the experiments using 129S6 mice as judges and found a significant overall interaction (P = 0.034), but only one stimulus pairing reached significance on its own (BALB/c vs. 129S6, P = 0.0021). These data suggest that a characteristic pattern of exploration in B6 mice can distinguish some socially atypical animals from controls. En ligne : http://dx.doi.org/10.1002/aur.1280 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=202

Letting a Typical Mouse Judge whether Mouse Social Interactions Are Atypical / Charisma R. SHAH in Autism Research, 8-1 (February 2015)  

Public ISBD [article]  inAutism Research > 8-1 (February 2015) . - p.120-120 Titre : Letting a Typical Mouse Judge whether Mouse Social Interactions Are Atypical Type de document : texte imprimé Auteurs : Charisma R. SHAH, Auteur ; Carl Gunnar FORSBERG, Auteur ; Jing-Qiong KANG, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur Article en page(s) : p.120-120 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.1321 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=256 [article] Letting a Typical Mouse Judge whether Mouse Social Interactions Are Atypical [texte imprimé] / Charisma R. SHAH, Auteur ; Carl Gunnar FORSBERG, Auteur ; Jing-Qiong KANG, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur . - p.120-120. Langues : Anglais (eng) in Autism Research > 8-1 (February 2015) . - p.120-120 Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1002/aur.1321 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=256

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