Sheryl S. Moy
University of North Carolina at Chapel Hill
121 Papers
1.1K Citations
Sheryl S. Moy is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Autism & Prepulse inhibition. The author has an hindex of 40, co-authored 110 publications.
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Papers
Phencyclidine supersensitivity in rats with neonatal dopamine loss
Sheryl S. Moy,George R. Breese +1 more
TL;DR: It is confirmed that rats with neonatal dopamine loss show enhanced sensitivity to NMDA antagonists, and may provide an animal model for the altered NMDA receptor function observed in human clinical syndromes.
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A de novo deafwaddler mutation of Pmca2 arising in ES cells and hitchhiking with a targeted modification of the Pparg gene.
Yau Sheng Tsai,Avani A. Pendse,Sheryl S. Moy,Ikuko Mohri,Antonio Perez,Jacqueline N. Crawley,Kinuko Suzuki,Nobuyo Maeda +7 more
TL;DR: Heterozygous mutants have normal movement and motor function but are severely deficient in hearing, and homozygous T692K Pmca2 mutants exhibit severe balance disorder, impaired neurologic reflexes, and motor coordination, and have profound hearing loss.
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Prosocial effects of an oxytocin metabolite, but not synthetic oxytocin receptor agonists, in a mouse model of autism
Sheryl S. Moy,Brian L. Teng,Viktoriya D. Nikolova,Natallia V. Riddick,Catherine Simpson,Amy Van Deusen,William P. Janzen,Maria F. Sassano,Cort A. Pedersen,Michael B. Jarstfer +9 more
TL;DR: Findings from a preclinical screening program to evaluate oxytocin receptor (OXTR) agonists and Oxytocin metabolites for potential clinical use as more optimal treatments suggest that the prosocial effects of oxytocine could be mediated by downstream activity of oxyocine metabolites, raising the possibility of new pathways to target for drug discovery relevant to ASD.
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Impaired acquisition and operant responding after neonatal dopamine depletion in rats
TL;DR: The results of this experiment showed that neonatal dopamine depletion does not lead to severe motor impairment or the inability to learn, but does disrupt the normal patterns of behavior associated with operant conditioning.
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Increased sensitivity to kainic acid in a genetic model of reduced NMDA receptor function
TL;DR: In this article, the effects of the highly selective kainate antagonist LY382884 on behavioral responses and induction of Fos after administration of kainic acid to wild type mice and mice with genetically reduced NMDA receptor expression (NR1(neo/neo)).
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