The N-methyl-D-aspartate (NMDA) receptors are a class of ionotropic glutamate receptors involved in long-term potentiation, synaptic plasticity, learning and memory. NMDA receptor (NMDAR) channels are heteromers composed of two NMDAR1 (GluN1; Grin1) subunits and one or more of the four NMDAR2 subunits: NMDAR2A (GluN2A; Grin2a), NMDAR2B (GluN2B; Grin2b), NMDAR2C (GluN2C; Grin2c) and/or NMDAR2D (GluN2D; Grin2d).
The three lines listed below are part of a series of transgenic mice with forebrain excitatory neuron over-expression of GluN2A, GluN2B or GluN2D chimeric subunits in which the endogenous C-terminal intracellular domain of each was replaced with another subunit. All three lines exhibit transgene expression that is highly enriched in the cortex, striatum and hippocampus, but not in hindbrain regions such as the cerebellum. The donating investigator reports the overexpression levels were not quantified - in part because endogenous GluN2 subunit levels vary among brain areas, ages and individuals; complicating expression level analysis. When hemizygous for their respective transgene, all three lines are reported to be viable, fertile and indistinguishable from wildtype littermates in growth, body weight, locomotor activity and anxiety. To date (June 2016), the phenotype of homozygous mice has not been characterized.
Stock No. 029151: Tg-GluN2A2B(CT) mice have forebrain excitatory neuron over-expression of GluN2A2B(CTR); a chimeric NMDA glutamate receptor composed of the Grin2a N-terminal and transmembrane domains fused to the Grin2b C-terminal intracellular domain. These mice exhibit enhanced long-term potentiation, long-term recognition memory and contextual fear conditioning.
Stock No. 029152: Tg-GluN2B2A(CT) mice have forebrain excitatory neuron over-expression of GluN2B2A(CTR); a chimeric NMDA glutamate receptor composed of the Grin2b N-terminal and transmembrane domains fused to the Grin2a C-terminal intracellular domain. These mice exhibit significantly impaired long-term depression resulting in impaired short-term recognition memory and impaired long-term cued fear conditioning.
