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

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: 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]

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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];