Stress at learning facilitates memory formation by regulating AMPA receptor trafficking through a glucocorticoid action

摘要: Stress and glucocorticoids (GCs) can facilitate memory formation. However, the molecular mechanisms mediating their effects are largely unknown. α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR) trafficking has been implicated in changes synaptic strength at central glutamatergic synapses associated with In cell cultures, corticosterone shown to condition of AMPAR GluA2 subunit. this study, we investigated involvement facilitation learning by stress. Using water maze spatial task involving different stress levels, mice trained under more stressful conditions (water 22°C) showed better memory, higher post-training than lower 30°C). Strikingly, facilitated was accompanied enhanced expression AMPARs that not observed less conditions. Interfering GC actions injecting synthesis inhibitor, metyrapone, blocked both induced learning. Intracerebroventricular infusion peptide, pep2m, blocks interfering interaction between N-ethylmaleimide-sensitive factor GluA2, impaired immediate performance as well long-term retrieval, supporting a causal role for stress-induced memory. Evidence neural adhesion molecule N-cadherin is also provided. These findings underscore new mechanism whereby improve function.