Journal article
MK-801 impairs working memory on the Trial-Unique Nonmatch-to-Location test in mice, but this is not exclusively mediated by NMDA receptors on PV plus interneurons or forebrain pyramidal cells
Elysia Sokolenko, Jess Nithianantharajah, Nigel C Jones
Neuropharmacology | PERGAMON-ELSEVIER SCIENCE LTD | Published : 2020
Abstract
NMDA receptors (NMDAr) 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 NMDAr 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 gene encoding the obligatory subunit of the NMDAr - from PV + interneurons or CaMKIIα+ pyramidal cells using Cre-lox technology. Adult male PV GluN1 K..
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Awarded by Australian Research Council
Funding Acknowledgements
This work was supported by funding from the Australian Research Council (FT130100100, FT140101327).