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A spatial model of autophosphorylation of Ca<sup>2+</sup>/calmodulin-dependent protein kinase II (CaMKII) predicts that the lifetime of phospho-CaMKII after induction of synaptic plasticity is greatly prolonged by CaM-trapping.


ABSTRACT: Long-term potentiation (LTP) is a biochemical process that underlies learning in excitatory glutamatergic synapses in the Central Nervous System (CNS). The critical early driver of LTP is autophosphorylation of the abundant postsynaptic enzyme, Ca2+/calmodulin-dependent protein kinase II (CaMKII). Autophosphorylation is initiated by Ca2+ flowing through NMDA receptors activated by strong synaptic activity. Its lifetime is ultimately determined by the balance of the rates of autophosphorylation and of dephosphorylation by protein phosphatase 1 (PP1). Here we have modeled the autophosphorylation and dephosphorylation of CaMKII during synaptic activity in a spine synapse using MCell4, an open source computer program for creating particle-based stochastic, and spatially r

SUBMITTER: Bartol TM 

PROVIDER: S-EPMC10862815 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature