Synaptic plasticity rules with physiological calcium levels.
Ontology highlight
ABSTRACT:
SUBMITTER: Inglebert Y
PROVIDER: S-EPMC7777146 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Li2012 Calcium mediated synaptic
plasticity
This model is an extension of
BIOMD0000000183.
This model is described in the article:
Calcium input frequency,
duration and amplitude differentially modulate the relative
activation of calcineurin and CaMKII.
Li L, Stefan MI, Le Novère
N.
PLoS ONE 2012; 7(9): e43810
Abstract:
NMDA receptor dependent long-term potentiation (LTP) and
long-term depression (LTD) are two prominent forms of synaptic
plasticity, both of which are triggered by post-synaptic
calcium elevation. To understand how calcium selectively
stimulates two opposing processes, we developed a detailed
computational model and performed simulations with different
calcium input frequencies, amplitudes, and durations. We show
that with a total amount of calcium ions kept constant, high
frequencies of calcium pulses stimulate calmodulin more
efficiently. Calcium input activates both calcineurin and
Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) at all
frequencies, but increased frequencies shift the relative
activation from calcineurin to CaMKII. Irrespective of
amplitude and duration of the inputs, the total amount of
calcium ions injected adjusts the sensitivity of the system to
calcium input frequencies. At a given frequency, the quantity
of CaMKII activated is proportional to the total amount of
calcium. Thus, an input of a small amount of calcium at high
frequencies can induce the same activation of CaMKII as a
larger amount, at lower frequencies. Finally, the extent of
activation of CaMKII signals with high calcium frequency is
further controlled by other factors, including the availability
of calmodulin, and by the potency of phosphatase
inhibitors.
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2024-09-02 | BIOMD0000000628 | BioModels