Bertram2002_Gprotein_SynapticSignal

ABSTRACT:

This a model from the article:
Role for G protein Gbetagamma isoform specificity in synaptic signal processing:a computational study.
Bertram R, Arnot MI, Zamponi GW. J Neurophysiol 2002 May;87(5):2612-23 11976397 ,
Abstract:
Computational modeling is used to investigate the functional impact of Gprotein-mediated presynaptic autoinhibition on synaptic filtering properties. Itis demonstrated that this form of autoinhibition, which is relieved bydepolarization, acts as a high-pass filter. This contrasts with vesicledepletion, which acts as a low-pass filter. Model parameters are adjusted toreproduce kinetic slowing data from different Gbetagamma dimeric isoforms, whichproduce different degrees of slowing. With these sets of parameter values, wedemonstrate that the range of frequencies filtered out by the autoinhibitionvaries greatly depending on the Gbetagamma isoform activated by theautoreceptors. It is shown that G protein autoinhibition can enhance the spatialcontrast between a spatially distributed high-frequency signal and surroundinglow-frequency noise, providing an alternate mechanism to lateral inhibition. Itis also shown that autoinhibition can increase the fidelity of coincidencedetection by increasing the signal-to-noise ratio in the postsynaptic cell. Thefilter cut, the input frequency below which signals are filtered, depends onseveral biophysical parameters in addition to those related to Gbetagammabinding and unbinding. By varying one such parameter, the rate at whichtransmitter unbinds from autoreceptors, we show that the filter cut can beadjusted up or down for several of the Gbetagamma isoforms. This allows forgreat synapse-to-synapse variability in the distinction between signal andnoise.

This model was taken from the CellML repository and automatically converted to SBML.
The original model was: Bertram R, Arnot MI, Zamponi GW. (2002) - version=1.0
The original CellML model was created by:
Catherine Lloyd
[e-mail]
The University of Auckland

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ORGANISM(S): Homo sapiens

SUBMITTER: Camille Laibe 

PROVIDER: MODEL1006230024 | biostudies-other |

SECONDARY ACCESSION(S): 11976397

REPOSITORIES: biostudies-other