Abstract
The exact mechanism that underlies memory is still one of the biggest unresolved mysteries in neuroscience. However, a strong candidate for this memory mechanism is the activity-based strengthening of synapses known as long-term potentiation (LTP). Calcium/calmodulin-dependent protein kinase II (CaMKII), an important molecule for the induction of LTP, has been shown to play an important role in the maintenance of LTP and, as a result, is thought to be crucial for the process of memory storage. The importance of CaMKII in memory maintenance has not been verified on a behavioral level. Here we show that the transient expression of a dominant-negative form of CaMKII results in the erasure of a behavioral memory. Erasure of the memory persists after the expression of the mutant has ceased; suggesting that a maintenance process mediated by CaMKII was disrupted. To further investigate the role of CaMKII in memory, a constitutively activated form of CaMKII was expressed in the hippocampus in order to occlude memory. Expression of the activated form of CaMKII did, in fact, cause memory deficits thus providing more evidence to the theory that CaMKII plays an essential role in memory.