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Hayer2005_AMPAR_traff_model1

ABSTRACT: This is the basic model of AMPAR trafficking bistability. It is based on Hayer and Bhalla, PLoS Comput. Biol. 2005. It includes the degradation and turnover of AMPARs. The CaMKII portion of the model is not bistable. This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information. In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not.. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

SUBMITTER: Sharat Vayttaden  

PROVIDER: MODEL9086518048 | BioModels | 2005-01-01

REPOSITORIES: BioModels

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Publications

Molecular switches at the synapse emerge from receptor and kinase traffic.

Hayer Arnold A   Bhalla Upinder S US  

PLoS computational biology 20050729 2

Changes in the synaptic connection strengths between neurons are believed to play a role in memory formation. An important mechanism for changing synaptic strength is through movement of neurotransmitter receptors and regulatory proteins to and from the synapse. Several activity-triggered biochemical events control these movements. Here we use computer models to explore how these putative memory-related changes can be stabilised long after the initial trigger, and beyond the lifetime of synaptic  ...[more]

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