Mice hemizygous for the human Thy-1-COX-2 transgene (hCOX-2 transgene) are viable and fertile, with expression of human COX-2 (<i>PTGS2</i> or PGE2) directed primarily to neurons of the amygdala, striatum, cerebral cortex, and hippocampus by the murine Thy1.2 expression cassette. These overexpressing C57BL/6J COX-2 transgenic line 303 mice have PGE2 levels that are ~25-40-fold greater than non-transgenic controls (compared to ~10-12-fold overexpression in line 300; see Stock No. <a href="https://www.jax.org/strain/010800">010800</a>). At approximately 12 months of age, COX-2 transgenic mice develop an age-dependent deficit in spatial memory. Around 20 months of age, a less pronounced, but significant deterioration in performance of non-spatial memory tasks develops. Further progressive memory impairments are observed over time. These cognitive deficits are associated with parallel age-dependent increases in cortical neuronal apoptosis and glial activation. Transgenic mice exhibit enhanced hippocampal longterm synaptic plasticity. Chronic overexpression of neuronal COX-2 enzymatic activity leads to long-term cellular changes that result in diminished neuron viability in transient focal ischemia/ischemic injury challenge. Elevated expression of COX-2 leads to increased oxidative degradation of endocannabinoids (eCBs) resulting in abolished depolarization-induced suppression of inhibition (DSI; or eCB-induced suppression of GABAergic synaptic transmission). These human Thy-1-COX-2 transgenic mice may be useful to model chronic elevations in COX-2 enzymatic activity associated with neurodegenerative diseases and aging, oxidative metabolism of endocannabinoids in modulation of synaptic transmission and plasticity, and ischemia and postischemic inflammatory reaction.

These human Thy-1-COX-2 transgenic mice express human COX-2 (<i>PTGS2</i> or PGE2)  primarily in neurons of the amygdala, striatum, cerebral cortex, and hippocampus as directed by the murine Thy1.2 expression cassette. These overexpressing COX-2 transgenic mice exhibit PGE2 levels that are ~25-40-fold greater than non-transgenic controls. 


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