Radke Anna K, Jury Nicholas J, Delpire Eric, Nakazawa Kazu, Holmes Andrew
Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA.
Alcohol. 2017 Feb;58:47-51. doi: 10.1016/j.alcohol.2016.07.005. Epub 2016 Aug 12.
N-Methyl-d-aspartate receptors (NMDAR) are involved in the regulation of alcohol drinking, but the contribution of NMDAR subunits located on specific neuronal populations remains incompletely understood. The current study examined the role of GluN2B-containing NMDARs expressed on cortical principal neurons and cortical interneurons in mouse ethanol drinking. Consumption of escalating concentrations of ethanol was measured in mice with GluN2B gene deletion in either cortical principal neurons (GluN2B) or interneurons (GluN2B), using a two-bottle choice paradigm. Results showed that GluN2B, but not GluN2B, mice consumed significantly less ethanol, at relatively high concentrations, than non-mutant controls. In a second paradigm in which mice were offered a 15% ethanol concentration, without escalation, GluN2B mice were again no different from controls. These findings provide novel evidence for a contribution of interneuronal GluN2B-containing NMDARs in the regulation of ethanol drinking.
N-甲基-D-天冬氨酸受体（NMDAR）参与酒精摄入的调节，但位于特定神经元群体上的NMDAR亚基的作用仍未完全明确。本研究探讨了在小鼠乙醇摄入过程中，表达于皮质主神经元和皮质中间神经元上的含GluN2B的NMDAR的作用。采用双瓶选择范式，检测了皮质主神经元（GluN2B）或中间神经元（GluN2B）中GluN2B基因缺失的小鼠对浓度递增的乙醇的摄入量。结果显示，在相对高浓度时，GluN2B而非GluN2B小鼠的乙醇摄入量显著低于非突变对照组。在第二个范式中，给小鼠提供15%的乙醇浓度且不递增，GluN2B小鼠的乙醇摄入量与对照组再次无差异。这些发现为含GluN2B的中间神经元NMDAR在乙醇摄入调节中的作用提供了新证据。
