Letter to the EditorGlycinamide prevents MK-801-induced hyperactivity and deficits in object recognition memory in an animal model of positive and cognitive symptoms of schizophrenia
Section snippets
Role of the funding sources
Grants from the Consejo Nacional de Ciencia y Tecnología (CONACyT, México):
Funds from grant # 129381 (to KLH) were used to purchase reagents and other materials necessary to carry out the present experiments.
Funds from grant # 134291 (to OGF) were used to purchase equipment used in carrying out the present experiments.
Grant from the Secretaría de Educación Pública — Universidad Autónoma de Tlaxcala (grant # CACyPI UAT-2014) provided funds to purchase feed and other materials necessary for
Contributors
E Basurto and KL Hoffman designed the study and carried out the statistical analyses. E Basurto carried out all experiments, collected the data and wrote the first draft of the manuscript. OGF participated in discussions on the analyses of data and interpretation of results, and provided the space, animals, and equipment necessary to carry out the experiments. KLH prepared the final version of the manuscript, which was approved by all authors.
Conflict of interest
All authors declare that they have no conflicts of interest.
Acknowledgments
This work was supported by grants from the Consejo Nacional de Ciencia y Tecnología, México, to KLH (grant #129381) and OGF (#134291), and from the Secretaría de Educación Pública, México — Universidad Autónoma de Tlaxcala (grant #CACyPI UAT-2014).
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Clozapine and glycinamide prevent MK-801-induced deficits in the novel object recognition (NOR) test in the domestic rabbit (Oryctolagus cuniculus)
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Quercetin Reduces Cortical GABAergic Transmission and Alleviates MK-801-Induced Hyperactivity
2018, EBioMedicineCitation Excerpt :Consequently, the NMDAR antagonist such as MK-801 has been shown to induce hyperactivity using locomotor activity paradigm in rodents to model the part of the positive symptoms in psychosis [1, 23, 70, 71] for novel antipsychotic drug discovery [58] and therapeutic development [42–44]. Not surprisingly, agents potentiating glutamatergic transmission, by activating the glycine modulatory site on the NMDAR, have been reported to reduce some of the cognitive symptoms of schizophrenia [4, 14, 15]. Specifically, schizophrenia, particularly the cognitive symptoms of the disorder, may result from the low activity of NMDAR on the GABAergic inhibitory interneurons in the prefrontal cortex [10–12, 26, 42, 43, 46, 71], as the postnatal ablation of NMDAR in this subtype of neurons conferred most schizophrenia-like phenotypes [5, 20].
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