NMDA receptor subunits and associated signaling molecules mediating antidepressant-related effects of NMDA-GluN2B antagonism
作者: Carly KiselycznykNicholas J. JuryLindsay R. HalladayKazu NakazawaMasayoshi MishinaRolf SprengelSeth G.N. GrantPer SvenningssonAndrew Holmes
作者单位: 1Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA
2Department of Psychiatry and Behavioral Neurobiology, University of Alabama at Birmingham, Birmingham, AL, USA
3Brain Science Laboratory, The Research Organization of Science and Technology, Ritsumeikan University, Kusatsu, Shiga, Japan
4Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Heidelberg, Germany
5Genes to Cognition Program, Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK
6Laboratory of Translational Neuropharmacology, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden
刊名: Behavioural Brain Research, 2015, Vol.287 , pp.89-95
来源数据库: Elsevier Journal
DOI: 10.1016/j.bbr.2015.03.023
关键词: GlutamatePSD-95Prefrontal cortexGluN2BGluA1Depression
原始语种摘要: Abstract(#br)Drugs targeting the glutamate N -methyl- d -aspartate receptor (NMDAR) may be efficacious for treating mood disorders, as exemplified by the rapid antidepressant effects produced by single administration of the NMDAR antagonist ketamine. Though the precise mechanisms underlying the antidepressant-related effects of NMDAR antagonism remain unclear, recent studies implicate specific NMDAR subunits, including GluN2A and GluN2B, as well as the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR) subunit glutamate receptor interacting molecule, PSD-95. Here, integrating mutant and pharmacological in mice, we investigated the contribution of these subunits and molecules to antidepressant-related behaviors and the antidepressant-related effects of the GluN2B...
全文获取路径: Elsevier  (合作)
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影响因子:3.327 (2012)

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