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dc.contributor.authorCui, Yihui
dc.contributor.authorJin, Jing
dc.contributor.authorZhang, Xuliang
dc.contributor.authorXu, Hao
dc.contributor.authorYang, Liguo
dc.contributor.authorDu, Dan
dc.contributor.authorZeng, Qingwen
dc.contributor.authorTsien, Joe Z.
dc.contributor.authorYu, Huiting
dc.contributor.authorCao, Xiaohua
dc.date.accessioned2012-10-26T16:27:00Z
dc.date.available2012-10-26T16:27:00Z
dc.date.issued2011-05-31en_US
dc.identifier.citationPLoS One. 2011 May 31; 6(5):e20312en_US
dc.identifier.issn1932-6203en_US
dc.identifier.pmid21655294en_US
dc.identifier.doi10.1371/journal.pone.0020312en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/655
dc.description.abstractPrefrontal cortex plays an important role in working memory, attention regulation and behavioral inhibition. Its functions are associated with NMDA receptors. However, there is little information regarding the roles of NMDA receptor NR2B subunit in prefrontal cortical synaptic plasticity and prefrontal cortex-related working memory. Whether the up-regulation of NR2B subunit influences prefrontal cortical synaptic plasticity and working memory is not yet clear. In the present study, we measured prefrontal cortical synaptic plasticity and working memory function in NR2B overexpressing transgenic mice. In vitro electrophysiological data showed that overexpression of NR2B specifically in the forebrain region resulted in enhancement of prefrontal cortical long-term potentiation (LTP) but did not alter long-term depression (LTD). The enhanced LTP was completely abolished by a NR2B subunit selective antagonist, Ro25-6981, indicating that overexpression of NR2B subunit is responsible for enhanced LTP. In addition, NR2B transgenic mice exhibited better performance in a set of working memory paradigms including delay no-match-to-place T-maze, working memory version of water maze and odor span task. Our study provides evidence that NR2B subunit of NMDA receptor in prefrontal cortex is critical for prefrontal cortex LTP and prefrontal cortex-related working memory.
dc.rightsCui et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.subjectResearch Articleen_US
dc.subjectBiologyen_US
dc.subjectNeuroscienceen_US
dc.subjectAnimal Cognitionen_US
dc.subjectBehavioral Neuroscienceen_US
dc.subjectLearning and Memoryen_US
dc.titleForebrain NR2B Overexpression Facilitating the Prefrontal Cortex Long-Term Potentiation and Enhancing Working Memory Function in Miceen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3105019en_US
dc.contributor.corporatenameBrain & Behavior Discovery Institute
dc.contributor.corporatenameDepartment of Neurology
refterms.dateFOA2019-04-10T00:28:19Z
html.description.abstractPrefrontal cortex plays an important role in working memory, attention regulation and behavioral inhibition. Its functions are associated with NMDA receptors. However, there is little information regarding the roles of NMDA receptor NR2B subunit in prefrontal cortical synaptic plasticity and prefrontal cortex-related working memory. Whether the up-regulation of NR2B subunit influences prefrontal cortical synaptic plasticity and working memory is not yet clear. In the present study, we measured prefrontal cortical synaptic plasticity and working memory function in NR2B overexpressing transgenic mice. In vitro electrophysiological data showed that overexpression of NR2B specifically in the forebrain region resulted in enhancement of prefrontal cortical long-term potentiation (LTP) but did not alter long-term depression (LTD). The enhanced LTP was completely abolished by a NR2B subunit selective antagonist, Ro25-6981, indicating that overexpression of NR2B subunit is responsible for enhanced LTP. In addition, NR2B transgenic mice exhibited better performance in a set of working memory paradigms including delay no-match-to-place T-maze, working memory version of water maze and odor span task. Our study provides evidence that NR2B subunit of NMDA receptor in prefrontal cortex is critical for prefrontal cortex LTP and prefrontal cortex-related working memory.


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