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In long-term potentiation (LTP), one of the most studied types of neuralplasticity, synaptic strength is persistently increased in response tostimulation. Although a number of different proteins have been implicated inthe sub-cellular molecular processes underlying induction and maintenance ofLTP, the precise mechanisms remain unknown. A particular challenge is todemonstrate that a proposed molecular mechanism can provide the level ofstability needed to maintain memories for months or longer, in spite of thefact that many of the participating molecules have much shorter life spans.Here we present a computational model that combines simulations of severalbiochemical reactions that have been suggested in the LTP literature and showthat the resulting system does exhibit the required stability. At the core ofthe model are two interlinked feedback loops of molecular reactions, oneinvolving the atypical protein kinase PKM{\zeta} and its messenger RNA, theother involving PKM{\zeta} and GluA2-containing AMPA receptors. We demonstratethat robust bistability - stable equilibria both in the synapse's potentiatedand unpotentiated states - can arise from a set of simple molecular reactions.The model is able to account for a wide range of empirical results, includinginduction and maintenance of late-phase LTP, cellular memory reconsolidationand the effects of different pharmaceutical interventions.

Coupled feedback loops maintain synaptic long-term potentiation: A computational model of PKMzeta synthesis and AMPA receptor trafficking