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Sociality deficits in serine racemase knockout mice

BACKGROUND: Studies of schizophrenia have pointed to the role of glutamate in its pathophysiology. Mice lacking D‐serine show impairments in neurotransmission through NMDA receptors and display behaviors consistent with features of schizophrenia. Yet, socio‐communicative deficits, a characteristic o...

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Detalles Bibliográficos
Autores principales: Matveeva, Tatyana M., Pisansky, Marc T., Young, Amy, Miller, Robert F., Gewirtz, Jonathan C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6790321/
https://www.ncbi.nlm.nih.gov/pubmed/31515952
http://dx.doi.org/10.1002/brb3.1383
Descripción
Sumario:BACKGROUND: Studies of schizophrenia have pointed to the role of glutamate in its pathophysiology. Mice lacking D‐serine show impairments in neurotransmission through NMDA receptors and display behaviors consistent with features of schizophrenia. Yet, socio‐communicative deficits, a characteristic of schizophrenia, have not been reported in serine racemase knockout mice. METHODS: We use behavioral testing (the three‐chambered social approach task, the dyadic interaction task, and the novel object recognition task) to examine socio‐communicative behaviors in these mice. RESULTS: Serine racemase mice show abnormal social investigation and approach behavior, and differ from wild‐type controls in the duration and number of vocalizations they emit in the presence of a conspecific. Serine racemase knockout mice were not impaired in a cognitive test (novel object recognition), although they displayed abnormal behavior in the acquisition phase of the task. CONCLUSIONS: Serine racemase knockout mice demonstrate abnormalities in socio‐communicative behaviors consistent with an impairment in sociality, a negative symptom of schizophrenia.