Acutely increasing alpha calcium/calmodulin-dependent protein kinase II in lateral amygdala enhances auditory fear conditioning memory

Alpha calcium/calmodulin-dependent protein kinase II (alphaCaMKII) is a calcium-activated enzyme that is highly expressed in the brain. Previous studies show that disrupting alphaCaMKII function impairs several forms of memory. In the present study we assessed the effects of locally increasing alphaCaMKII levels on memory. To this end, we used a replication-defective herpes simplex viral (HSV) vector to express alphaCaMKII or control vectors into the lateral amygdala (LA), a region known to be critical for auditory fear memory. Mice received bilateral microinfusion of HSV vectors aimed at the LA 2 days before fear conditioning training. During fear conditioning a tone was paired with a shock. Memory was assessed 24 hours following training as the percentage of time spent freezing during subsequent tone presentation. We found that acutely increasing aCaMKII levels in LA neurons enhanced auditory fear memory. Importantly, locomotor activity and anxiety behaviour were not altered by overexpression of alphaCaMKII, suggesting that the observed increase in fear memory cannot be attributed to a non-specific increase in anxiety. These findings indicate that local and acute overexpression of alphaCaMKII enhances fear memory.