These NMDAR1-loxP mice possess loxP sites flanking exons 9-10 of the glutamate receptor, ionotropic, NMDA1 (zeta 1) (Grin1) gene, approximately 2.1 kbp of sequence. GRIN1 encodes a subunit of N-methyl-D-aspartate receptors which form ligand-gated ion channels that play a key role in the plasticity of synapses. Mice that are homozygous for this allele are viable and fertile. When bred to Ppp1r2-Cre mice (Stock No. <a href="https://www.jax.org/strain/012686">012686</a>), expressing cre in corticolimbic GABAergic interneurons, resulting knock-out mice exhibit an elimination of Grin1 transcripts in 40-50% of cortical and hippocampal interneurons, mostly parvalbuin-positive, during early postnatal development. They have abolished NMDAR mediated currentscurrents from GABAergic neurons in medial PFC (mPFC), neocortex and hippocampus, while NMDA currents in cortical pyramidal neurons were unaffected. Distinct schizophrenia-related symptoms emerge after adolescence, including novelty-induced hyperlocomotion, mating and nest-building deficits, as well as anhedonia-like and anxiety-like behaviors. Many of these behaviors are exacerbated by social isolation stress. Social memory, spatial working memory, and prepulse inhibition are also impaired. Reduced expression of glutamic acid decarboxylase and parvalbumin is accompanied by disinhibition of cortical excitatory neurons and reduced neuronal synchrony. Moreover, amphetamine-induced dopamine release was enhanced in nucleus accumbens, whereas it was dramatically reduced in mPFC compared to controls, mimicking dopamine abnormality in patients with schizophrenia. Of note, another floxed strain, with exons 11-21 floxed, is available as Stock No. <a href="https://www.jax.org/strain/005246">005246</a>. Cre excision of exon 11-21 deletes a 12 kb segment of the gene, while breeding to a cre line only removes a 2.1kb segment in Stock No. 036352. When bred to Ppp1r2-Cre mice, ablation of Grin1 transcripts in corticolibmic GABAergic neurons begins at 8 weeks of age and is completed by 20 weeks old, and they show almost no schizophrenia-like phenotypes.

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These NMDAR1-loxP mice possess loxP sites flanking exons 9-10 of the Grin1 gene. These mice may be useful in studying the NMDAR and its downstream signaling molecules/pathways, synaptic plasticity, and social behavior.

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