The wide-spread idea that CAMKII would somehow, just by being activated, form long term memory, by as acting as a molecular switch that can store information indefinitely (Lisman, 1985)^[1], shows just how strong the empirical correlation has been between CAMKII and memory, seen in how genetic deletion of CAMKII impairs long term memory, how CAMKII is most concentrated in the hippocampus and cortex - there was enough evidence to justify the somewhat nonsensical idea that this Type II CaM kinase formed a bistable molecular switch, a transistor,^{[1, 2]} in the absence of a molecular switch, one had to be made up.

In 2012, almost three decades after John E Lisman proposed that memory was the result of an autophosphorylating kinase and a molecular switch^[1], a new model from Craddock, Tuszynski, and Hameroff shows that rather than CAMKII acting as a bistable switch in itself (not even possible to begin with), it is acting as an intermediary, switching the state of tubulins as molecular switches, and encoding memory in microtubule lattices.^[3]

References

1. A Mechanism for Memory Storage Insensitive to Molecular Turnover: A Bistable Autophosphorylating Kinase (1985)

2. Regulation of Brain Type II Ca2+/CalmodulinDependent Protein Kinase by Autophosphorylation: A Ca2+-Triggered Molecular Switch (1986)

3. Cytoskeletal Signaling: Is Memory Encoded in Microtubule Lattices by CaMKII Phosphorylation? (2012)