Reduced spontaneous activity of mice defective in the ε4 subunit of the NMDA receptor channel
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Loss of the sustained antidepressant-like effect of (2R,6R)-hydroxynorketamine in NMDA receptor GluN2D subunit knockout mice
2024, Journal of Pharmacological SciencesQuantitative analysis of NMDA receptor subunits proteins in mouse brain
2023, Neurochemistry InternationalMultiple roles of GluN2D-containing NMDA receptors in short-term potentiation and long-term potentiation in mouse hippocampal slices
2021, NeuropharmacologyCitation Excerpt :Dysregulation of GluN2D-containing NMDARs is also likely to be involved in a variety of disorders. GluN2D KO mice (Ikeda et al., 1995) possess a number of interesting phenotypes, such as lack of phencyclidine-induced hyperlocomotor activity (Hagino et al., 2010). This observation indicated that GluN2D may be an important site of action of the uncompetitive NMDAR channel blockers.
Clinical and therapeutic significance of genetic variation in the GRIN gene family encoding NMDARs
2021, NeuropharmacologyCitation Excerpt :Although Grin2b knockout mice do breathe, they do not suckle and thus do not survive the neonatal period. The homozygous null mutations of Grin2a (Sakimura et al., 1995; Kadotani et al., 1996), Grin2c (Ebralidze et al., 1996), and Grin2d (Ikeda et al., 1995a) appear less severe than those homozygous null Grin1 and Grin2b mice, with each being fertile and viable, albiet with abberations in a variety of behavoiral and cognitive tasks (Camp and Yuan, 2020; Boyce-Rustay and Holmes, 2006; Brigman et al., 2008; Bannerman et al., 2008; Hillman et al., 2011; Shelkar et al., 2019; Yamamoto et al., 2017; Salimando et al., 2020). However, these characterizations largely preceded an appreciation of the scope of GRIN disorders, and additional study of null mutations, especially in heterozygous animals, could provide meaningful insights into the impact of LoF GRIN variants.
GRIN2D/GluN2D NMDA receptor: Unique features and its contribution to pediatric developmental and epileptic encephalopathy
2020, European Journal of Paediatric Neurology
- 1
Present address: Laboratory for Synaptic Function, Institute of Physical and Chemical Research, Saitama 351-01, Japan.
- 2
Present address: Laboratory of Neurobiology and Behavioral Genetics, National Institute for Physiological Sciences, Okazaki 444, Japan.
- 3
Present address: Laboratory of Morphogenesis, Institute of Molecular Embryology and Genetics, Kumamoto University School of Medicine, Kumamoto 860, Japan.