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MODEL1505130001 - Jalil2015 - Atypical protein kinase C isoforms in memory maintenance (Model2)


The following model is part of the non-curated branch of BioModels Database. While the syntax of the model has been verified, its semantics remains unchecked. Any annotation present in the models is not a product of BioModels' annotators. We are doing our best to incorporate this model into the curated branch as soon as possible. In the meantime, we display only limited metadata here. For further information about the model, please download the SBML file.

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Reference Publication
Publication ID: 26077687
Jalil SJ, Sacktor TC, Shouval HZ.
Atypical PKCs in memory maintenance: the roles of feedback and redundancy.
Learn. Mem. 2015 Jul; 22(7): 344-353
Department of Neurobiology and Anatomy, The University of Texas Medical School at Houston, Houston, Texas 77030, USA.  [more]
Original Model: MODEL1505130001.origin
Submitter: Sajiya Jalil
Submission Date: 13 May 2015 15:04:06 UTC
Last Modification Date: 04 Dec 2015 16:10:23 UTC
Creation Date: 04 Dec 2015 11:35:07 UTC
Encoders:  Sajiya Jalil
Jalil2015 - Atypical protein kinase C isoforms in memory maintenance (Model2)

This is a non-SBML model

This model is not available in SBML, the SBML that is provided here is a dummy model. The author (Sajiya Jalil), sent the matlab code of two models (MODEL1505130000-1), and wanted them to be deposited in BioModels. As the models could not be currently implemented in SBML, we generated dummy SBML files for now. Click here to download the matlab file of the model, which generates the figures in the main paper.

This model is described in the article:

Jalil SJ, Sacktor TC, Shouval HZ.
Learn. Mem. 2015 Jul; 22(7): 344-353


Memories that last a lifetime are thought to be stored, at least in part, as persistent enhancement of the strength of particular synapses. The synaptic mechanism of these persistent changes, late long-term potentiation (L-LTP), depends on the state and number of specific synaptic proteins. Synaptic proteins, however, have limited dwell times due to molecular turnover and diffusion, leading to a fundamental question: how can this transient molecular machinery store memories lasting a lifetime? Because the persistent changes in efficacy are synapse-specific, the underlying molecular mechanisms must to a degree reside locally in synapses. Extensive experimental evidence points to atypical protein kinase C (aPKC) isoforms as key components involved in memory maintenance. Furthermore, it is evident that establishing long-term memory requires new protein synthesis. However, a comprehensive model has not been developed describing how these components work to preserve synaptic efficacies over time. We propose a molecular model that can account for key empirical properties of L-LTP, including its protein synthesis dependence, dependence on aPKCs, and synapse-specificity. Simulations and empirical data suggest that either of the two aPKC subtypes in hippocampal neurons, PKMζ and PKCι/λ, can maintain L-LTP, making the system more robust. Given genetic compensation at the level of synthesis of these PKC subtypes as in knockout mice, this system is able to maintain L-LTP and memory when one of the pathways is eliminated.

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.