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https://www.selleckchem.com/products/triptolide.html RESULTS Neuronal activity and orientation/direction selectivity were unaffected in Setd1a+/- mice, but correlations between cell pairs in V1 showed altered distributions compared with wild-type mice, in both ongoing and visually evoked activity. Furthermore, population-wide "ensemble activations" in Setd1a+/- mice were markedly less reliable over time during rest and visual stimulation, resulting in unstable encoding of basic visual information. This alteration of ensembles coincided with reductions in alpha and high-gamma band phase synchrony within and between cortical layers. CONCLUSIONS These results provide new evidence for an ensemble hypothesis of schizophrenia and highlight the utility of Setd1a+/- mice for modeling sensory-processing phenotypes. Published by Elsevier Inc.BACKGROUND 22q11.2 deletions and duplications are copy number variations (CNVs) that predispose to developmental neuropsychiatric disorders. Both CNVs are associated with autism spectrum disorder (ASD), while the deletion confers disproportionate risk for schizophrenia. Neurobehavioral profiles associated with these reciprocal CNVs in conjunction with brain imaging measures have not been reported. METHODS We profiled the impact of 22q11.2 CNVs on neurobehavioral measures relevant to ASD and psychosis in 106 22q11.2 deletion carriers, 38 22q11.2 duplication carriers, and 82 demographically matched healthy control subjects. To determine whether brain-behavior relationships were altered in CNV carriers, we further tested for interactions between group and regional brain structure on neurobehavioral domains. RESULTS Cognitive deficits were observed in both CNV groups, with the lowest IQs in deletion carriers. ASD and dimensionally measured ASD traits were elevated in both CNV groups; however, duplication carriers exhibited increased stereotypies compared to deletion carriers. Moreover, discriminant analysis using ASD subdomains distinguished

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