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      Glycine transporter inhibition reverses ketamine-induced working memory deficits.

      Neuroreport

      Treatment Outcome, Analysis of Variance, Tantalum, Schizophrenia, Potassium, Oxides, therapeutic use, Nootropic Agents, Neuropsychological Tests, drug effects, Memory, Short-Term, drug therapy, chemically induced, Memory Disorders, Macaca mulatta, Imidazoles, Hallucinations, antagonists & inhibitors, Glycine Plasma Membrane Transport Proteins, Female, Disease Models, Animal, Azabicyclo Compounds, Animals

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          Abstract

          Glycine transporter inhibitors have recently been reported to improve symptoms in patients with schizophrenia. Here we used acute ketamine in the nonhuman primate to test the effectiveness of the novel glycine transporter inhibitor, PF-3463275, in a model of cognitive dysfunction relevant to schizophrenia. PF-3463275 (0.01-0.17 mg/kg; subcutaneously) or a vehicle was given before the administration of ketamine (median dose of 1.0 mg/kg intramuscularly) or placebo (saline). Ketamine induced hallucinatory-like behaviors that were not reversed by PF-3463275. In contrast, all doses of PF-3463275 alleviated the deficit in spatial working memory induced by ketamine. Theses findings build upon those in patients by providing translational support for targeting glycine transporter in adjunctive treatment for cognitive dysfunction in schizophrenia.

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          Journal
          20186106
          10.1097/WNR.0b013e3283381a4e

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