| Abstract: |
| Based on the physiological mechanism underlying the hippocampus for memory storage, we have developed a CA3CA1 synaptic network memory model that elucidates the stored process of sensory information. Once information is stored in long-term memory, the model encodes it into trajectories within a stable heteroclinic network (SHN) in the phase space. Saddle points within the SHN represent the information blocks that information is divided into in the process of short-term memory. In this paper, memory strength and lifetime are introduced to measure the stability of memory storage in hippocampus. We track the storage process of initial memory, which is stored in distinct synaptic pattern, resulting in a durable memory engram. Subsequent memories are stored in either tracked or untracked synapses, which can cause decay and interference on the engram of the initial memory. We discussed the dynamics of AMPA receptors efficacy on tracked synapses based on the CA3CA1 synaptic network model. And estimated the decay effect of untracked synapses based on a synaptic plasticity discrete model. Numerical results indicate that the memory strength is dependent on the relative activation level of the PKA cascade within the postsynaptic neurons during encoding. This strength is further augmented during the consolidation process, which is induced by the decay effect. In the process of consolidation, the complexity of information and the number of synaptic inputs, as well as the excitatory-inhibitory balance, are important factors influencing the memory strength. The forgetting process for long-term memory is driven by the decay effect, and the memory information, efficiency, and various neurodegenerative diseases can alter the lifetime of initial memory by regulating the decay effect. |
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