Multiple mechanisms of short term plasticity at the calyx of Held (Hennig et al. 2008)

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Accession:113649
This is a new model of the short-term dynamics of glutamatergic synaptic transmission, which incorporates multiple mechanisms acting at differing sites and across a range of different time scales (ms to tens of seconds). In the paper, we show that this model can accurately reproduce the experimentally measured time-course of short term depression across different stimulus frequencies at the calyx of Held. The model demonstrates how multiple forms of activity-dependent modulation of release probability and vesicle pool depletion interact, and shows how stimulus-history-dependent recovery from synaptic depression can arise from dynamics on multiple time scales.
Reference:
1 . Hennig MH, Postlethwaite M, Forsythe ID, Graham BP (2008) Interactions between multiple sources of short term plasticity during evoked and spontaneous activity at the rat calyx of Held J Physiol 586(13):3129-3146 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Synapse;
Brain Region(s)/Organism:
Cell Type(s): Medial Nucleus of the Trapezoid Body (MNTB) neuron;
Channel(s): I Calcium;
Gap Junctions:
Receptor(s): AMPA; mGluR;
Gene(s):
Transmitter(s): Glutamate;
Simulation Environment: MATLAB;
Model Concept(s): Short-term Synaptic Plasticity;
Implementer(s): Hennig, Matthias H [mhhennig at gmail.com];
Search NeuronDB for information about:  AMPA; mGluR; I Calcium; Glutamate;
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