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Takata, A.

Publications and source records attributed to Takata, A..

2 recordsLinked to original sources

Distinct Patterns of Adaptive Decision-Making in Mouse Models of Neurodevelopmental Disorders

Neurodevelopmental disorders (NDDs) arise from diverse genetic alterations that can affect adaptive decision-making, but quantifying specific components of cognitive processes remains challenging. We developed a sequence of deterministic and probabilistic reversal learning tasks using an automated operant platform and applied reinforcement-learning models to quantify latent cognitive processes in mice. We applied this framework to three genetic NDD models: Mecp2+/- (Rett syndrome), MECP2-Tg1 (MECP2 duplication syndrome), and Kmt2c+/fs (KMT2C haploinsufficiency) mice. Mecp2+/- mice showed heterogeneous impairment in acquiring deterministic reversal learning, accompanied by reduced task engagement and increased premature responses. MECP2-Tg1 mice exhibited mild impairment of deterministic reversal learning but preserved performance in probabilistic reversal learning. Although Kmt2c+/fs mice showed largely preserved behavioral performance, reinforcement-learning modeling revealed increased learning from unrewarded outcomes and faster forgetting of unchosen options, which were not apparent from overall performance. These findings demonstrate that combining quantitative reversal learning tasks with computational modeling can distinguish specific alterations in cognitive processes, providing an effective framework for characterizing cognitive dysfunction across mouse models of NDDs.

neuroscience↗

Recapitulation and reversal of schizophrenia-related phenotypes in Setd1a-deficient mice

SETD1A, a histone methyltransferase, is a key schizophrenia susceptibility gene. Mutant mice carrying a heterozygous loss-of-function mutation of the orthologous gene exhibit alterations in axonal branching and cortical synaptic dynamics, accompanied by specific deficits in working memory that recapitulates SCZ-related alterations. We show that Setd1a targets mostly enhancers and reveal a striking overlap between Setd1a and Mef2 chromatin targets. Setd1a targets are highly expressed in pyramidal neurons and enriched for genes with postnatally-biased expression involved in synaptic structure and function. Notably, evolutionary conserved Setd1a binding sites and target genes are strongly associated with neuropsychiatric genetic risk burden. Reinstating Setd1a expression in adulthood rescues working memory deficits. We identify LSD1 as a major demethylase counteracting the effects of Setd1a methyl transferase activity and show that LSD1 antagonism in adult Setd1a-deficient mice results in a full rescue of the behavioral abnormalities and axonal branching deficits. Our findings advance our understanding of how SETD1A mutations predispose to SCZ and point to therapeutic interventions.

neuroscience↗