https://www.selleckchem.com/products/shr0302.html
NMDA receptors are widely expressed throughout the brain on many cell types, and loss of function of these receptors (ie NMDAr hypofunction) is a candidate mechanism explaining working memory impairment in schizophrenia. However, the cellular source driving the working memory deficits caused by NMDA hypofunction has not been explored. The aim of this study was to assess the contribution of NMDAr on pyramidal cells and parvalbumin (PV+) interneurons to impairments in working memory induced by NMDAr hypofunction. We excised GluN1 - the ge
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