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

@entity4235 @entity39791 @entity21043 @entity19 @entity8816 @entity2819 @entity140 @entity9449
Stress and glucocorticoids (GCs) can facilitate memory formation. However, the molecular mechanisms mediating their effects are largely unknown. @entity140 ( @entity140 ) receptor (AMPAR) trafficking has been implicated in the changes in synaptic strength at central glutamatergic synapses associated with memory formation. In cell cultures, @entity2819 has been shown to condition the synaptic trafficking of the AMPAR @entity9449 subunit. In this study, we investigated the involvement of @entity9449 trafficking in the facilitation of learning by stress. Using the water maze spatial task involving different stress levels, @entity19 trained under more stressful conditions (water at 22 degrees C) showed better learning and memory, and higher post-training @entity2819 levels, than @entity19 trained under lower stress (water at 30 degrees C). Strikingly, this facilitated learning by stress was accompanied by enhanced synaptic expression of @entity9449 AMPARs that was not observed in @entity19 trained under less stressful conditions. Interfering with GC actions by injecting the GC synthesis inhibitor, @entity4235 , blocked both the memory facilitation and the enhanced @entity9449 trafficking induced by stressful learning. Intracerebroventricular infusion of the peptide, @entity39791 m, that blocks @entity9449 synaptic trafficking by interfering with the interaction between @entity8816 -sensitive factor and @entity9449 , impaired immediate performance at learning as well as long-term memory retrieval, supporting a causal role for @entity9449 trafficking in stress-induced facilitation of spatial learning and memory. Evidence for the involvement of the neural cell adhesion molecule @entity21043 in interaction with @entity9449 is also provided. These findings underscore a new mechanism whereby stress can improve memory function.
