Grin2b Conditional Knockout mouse models

GluN2B, encoded by Grin2b, the mouse ortholog of human GRIN2B, is the dominant NMDA receptor GluN2 subunit in embryonic and early postnatal brain, generating currents with slow deactivation and high charge transfer, and it is uniquely blocked by ifenprodil and related amino-terminal domain antagonists. Its exceptionally long cytoplasmic tail binds CaMKII with high affinity and scaffolds PSD-95 and SynGAP, so GluN2B is not merely a pore component but a signaling hub for synaptic plasticity and spine maturation. Constitutive nulls die perinatally with failed suckling and absent hippocampal long-term depression, which mandates floxed alleles combined with CaMKIIa-Cre or Emx1-Cre for adult work. Human GRIN2B variants cause intellectual disability and epileptic encephalopathy through both reduced current and gating gain of function, favoring targeted knockins, while tail-swap alleles separate ion flux from CaMKII recruitment. GluN2A upregulation partially masks loss, so measure ifenprodil-sensitive current directly rather than inferring composition.

Grin2b conditional knockout mice carry a floxed allele so you delete function only where Cre is active. The germline allele stays intact until you cross to a tissue specific Cre. Labs reach for this design when a global knockout is lethal, when they need adult onset loss, or when regional redundancy hides a whole body phenotype.