Abstract
People with schizophrenia (PWS), experience a reduced drive to engage in activity, despite potential benefits. Mechanisms underlying amotivated states remain unclear, but recent RDoC-based approaches enable disentanglement of motivation into component parts. PWS exhibit reduced effortful motivation and reward-related learning. Given that the transcription factor SP4 was identified linked to PWS via GWAS, we determined whether reduced Sp4 expression in mice would recreate these behaviors. Sp4 mice exhibit reduced NMDA1 receptor expression and since bromocriptine reversed NMDA disruption-induced deficits in working memory, we tested whether this dopamine D2 receptor (DRD2) agonist would normalize any amotivated-related behaviors.
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