1. Nakako T, Murai T, Ikejiri M, Hashimoto T, Kotani M, Matsumoto K, Manabe S, Ogi Y, Konoike N, Nakamura K, Ikeda K. {{Effects of lurasidone on ketamine-induced joint visual attention dysfunction as a possible disease model of autism spectrum disorders in common marmosets}}. {Behav Brain Res}. 2014.
Infants with autism have difficulties performing joint visual attention (JVA), defined as following another person’s pointing gesture and gaze. Some non-human primates (NHPs) can also perform JVA. Most preclinical research on autism spectrum disorders (ASD) has used rodents as animal models of this social interaction disorder. However, models using rodents fail to capture the complexity of social interactions that are disrupted in ASD. Therefore, JVA impairment in NHPs might be a more useful model of ASD. The aim of this study was to develop an appropriate and convenient ASD model with common marmosets. We first tested whether marmosets were capable of performing JVA. Subsequently, we administered ketamine, an N-methyl-D-aspartate (NMDA) receptor antagonist, to induce JVA impairment and investigated the effects of lurasidone, a newer antipsychotic agent, on the JVA impairments. An apparatus was constructed using 4 white boxes, which were attached to the corners of a frame. All boxes had a hinged door, and marmosets could easily obtain a reward by pushing the door. An experimenter pointed and gazed at the boxes to inform the marmosets which box contained the reward. Their behavior was scored according to the number of incorrect choices. The JVA score was significantly higher in the cued vs. uncued tasks. Ketamine significantly decreased the JVA score, but lurasidone significantly reversed this effect. These findings suggest that this experimental system could be a useful animal model of neuropsychiatric disorders characterized by NMDA-receptor signaling, including ASD, and that lurasidone might be effective for some aspects of ASD.
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2. Roser ME, Aslin RN, McKenzie R, Zahra D, Fiser J. {{Enhanced Visual Statistical Learning in Adults With Autism}}. {Neuropsychology}. 2014.
Objective: Individuals with autism spectrum disorder (ASD) are often characterized as having social engagement and language deficiencies, but a sparing of visuospatial processing and short-term memory (STM), with some evidence of supranormal levels of performance in these domains. The present study expanded on this evidence by investigating the observational learning of visuospatial concepts from patterns of covariation across multiple exemplars. Method: Child and adult participants with ASD, and age-matched control participants, viewed multishape arrays composed from a random combination of pairs of shapes that were each positioned in a fixed spatial arrangement. Results: After this passive exposure phase, a posttest revealed that all participant groups could discriminate pairs of shapes with high covariation from randomly paired shapes with low covariation. Moreover, learning these shape-pairs with high covariation was superior in adults with ASD than in age-matched controls, whereas performance in children with ASD was no different than controls. Conclusions: These results extend previous observations of visuospatial enhancement in ASD into the domain of learning, and suggest that enhanced visual statistical learning may have arisen from a sustained bias to attend to local details in complex arrays of visual features. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
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3. Rossignol R, Ranchon-Cole I, Paris A, Herzine A, Perche A, Laurenceau D, Bertrand P, Cercy C, Pichon J, Mortaud S, Briault S, Menuet A, Perche O. {{Visual sensorial impairments in neurodevelopmental disorders: evidence for a retinal phenotype in fragile x syndrome}}. {PLoS One}. 2014; 9(8): e105996.
Visual sensory impairments are common in Mental Deficiency (MD) and Autism Spectrum Disorder (ASD). These defects are linked to cerebral dysfunction in the visual cortical area characterized by the deregulation of axon growth/guidance and dendrite spine immaturity of neurons. However, visual perception had not been addressed, although the retina is part of the central nervous system with a common embryonic origin. Therefore, we investigated retinal perception, the first event of vision, in a murine model of MD with autistic features. We document that retinal function is altered in Fmr1 KO mice, a model of human Fragile X Syndrome. Indeed, In Fmr1 KO mice had a lower retinal function characterized by a decreased photoreceptors neuron response, due to a 40% decrease in Rhodopsin content and to Rod Outer Segment destabilization. In addition, we observed an alteration of the visual signal transmission between photoreceptors and the inner retina which could be attributed to deregulations of pre- and post- synaptic proteins resulting in retinal neurons synaptic destabilization and to retinal neurons immaturity. Thus, for the first time, we demonstrated that retinal perception is altered in a murine model of MD with autistic features and that there are strong similarities between cerebral and retinal cellular and molecular defects. Our results suggest that both visual perception and integration must be taken into account in assessing visual sensory impairments in MD and ASD.
