The NSE-hENT1 transgene contains a rat neuron-specific enolase (Eno2) promoter directing expression of a human solute carrier family 29 (nucleoside transporters), member 1 (SLC29A1 or ENT1). Expression is detected in the cerebral cortex, striatum, hippocampus and cerebellum, but not in skeletal muscle, heart, liver, kidney and lung. SLC29A1 is an equilibrative nucleoside transporter that mediates adenosine influx and efflux. Cortical synaptosomes exhibit increased [3H]adenosine uptake and [3H]nitrobenzylthioinosine binding. In response to caffeine administration, transgenic mice exhibit peak activity levels similar to wild-type, however, within 60 minutes there is a more rapid decrease in horizontal activity and fine movements. In response to ethanol administration, the duration of LORR (loss of righting response) is enhanced as compared to wild-type. In addition, mice exhibit reduced synaptic depression following hypoxia/ischemia and enhanced stroke injury. Both homozygote and hemizygote mice exhibit similar phenotypes, however, in biochemistry and some behavior experiments (ligand binding, western blot, qRT-PCR, ethanol-induced loss of righting response) homozygotes exhibit a greater magnitude of response. This strain may be useful for studying drug sensitivity and stroke.

The NSE-hENT1 transgene contains a rat neuron-specific enolase (Eno2) promoter directing expression of a human solute carrier family 29 (nucleoside transporters), member 1 (SLC29A1).  SLC29A1 or ENT1 mediates adenosine influx and efflux.  Transgenic mice exhibit altered responses to caffeine, alcohol, hypoxia and ischemia.

This strain is hosted by NIH's MMRRC, which partners with JAX for the distribution of this and other strains. For additional information and to purchase, please visit the MMRRC site.