Short-term memory is directly determined by the level of AMPA receptors (AMPARs) at the postsynaptic membrane, which is regulated by CaMKII and PSD-95. The constitutive AMPAR endocytosis and CaMKII inhibition are constantly erasing the short-term memory.
Long-term memory could be stored in the microtubule tracks (MTTs) transporting PSD-95 from the soma to the synapses. Once the MTTs are established, the synaptic strength can be maintained by PSD-95 expression at the soma, which is regulated by protein kinase C (PKC). The synaptic strength affects only the ability to recall an event, not the memory per se. Even after the synapses have been completely eliminated (e.g., by ischemia), memory can still be rescued by PKC activator (Sun et al., 2009).
Since long-term memory is stored in MTTs, the process of memory consolidation is to construct MTTs. This is initiated by spontaneous synaptic reactivation, resulting from CaMKII inhibition by CaMKIIN. MTTs will be (and should be) constructed only to the synapses which had been strongly stimulated, because only strong synaptic reactivation can send sufficient signals for the construction of MTTs.
Life review, a near-death experience, may also arise from synaptic reactivation. In a healthy brain, the synaptic reactivation caused by the tightly controlled CaMKII inhibition leads to the recall of a tiny fraction of life history. In near-death events (such as cardiac arrest or drowning), the ATP depletion may cause the exodus of CaMKII from most synapses, thereby resulting in the recall of most autobiographical memories.