TAT-GluA2 3Y

TAT-GluA2 3Y (4.32 μM/kg; intraperitoneal injection; single administration) blocks NLRP3 knockout-induced fear generalization in mice, restores the phosphorylation level of hippocampal AMPA receptor 1 at the ser831 site, and reduces phosphorylated CaMKII levels^[1].
TAT-GluA2 3Y (5 mg/kg; i.p.; multiple administrations) disrupts the interaction between Syt3 and GluA2, increases the surface expression level of GluA2, inhibits the formation of CP-AMPAR, reduces the cerebral ischemic volume by approximately 40%-50% in male SD rats with ischemic stroke induced by middle cerebral artery occlusion/reperfusion (MCAO/R), improves neurological function, and enhances the recovery of long-term sensorimotor and cognitive functions^[2].
TAT-GluA2 3Y (1.5 nM/g; intravenous injection; 5 times (once before each dexamphetamine injection, once every 2 days)) blocks the induction, maintenance and expression of amphetamine-induced behavioral and neurochemical sensitization in male SD rats^[4].
TAT-GluA2 3Y (15 pM; bilateral microinjection into the ventral tegmental area (VTA); 5 total injections, one before each d-amphetamine injection, once every 2 days) inhibits the maintenance and expression of amphetamine-induced behavioral sensitization in male SD rats, but does not inhibit its induction^[4].
Co-administration of TAT-GluA2 3Y (intravenously injected at a dose of 1.5-2.25 nM/g; administered 1 h prior to each morphine conditioning session) with morphine during the acquisition phase of morphine-conditioned place preference (CPP) promotes rapid extinction of preference, but does not affect the induction, expression, maintenance or reinstatement of CPP^[5].
TAT-GluA2 3Y (2.25 nM/g; intravenous injection; 1 hour prior to each food conditioning session) has no effect on the induction, extinction, or reinstatement of food-induced conditioned place preference in rats^[5].