['The labile state of short-term memory has been known for more than a century. It has been frequently reported that immediate postlearning intervention can readily disrupt newly formed memories. However, the molecular and cellular mechanisms underlying the labile state of new memory are not understood.', 'Using a bump-and-hole-based chemical-genetic method, we have rapidly and selectively manipulated alpha CaMKII activity levels in the mouse forebrain during various stages of the short-term memory processes. We find that a rapid shift in the alpha CaMKII activation status within the immediate 10 min after learning severely disrupts short-term memory formation. The same manipulation beyond the 15 min after learning has no effect, suggesting a critical time window for CaMKII action. We further show that during this same 10 min time window only, shifting in CaMKII activation state is capable of altering newly established synaptic weights and/or patterns.'] Does caMKII activation state underlie synaptic labile phase of LTP and short-term memory formation?