Models that contain the Cell : Medial Nucleus of the Trapezoid Body (MNTB) neuron

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    Models   Description
1.  Calyx of Held, short term plasticity (Yang Z et al. 2009)
This model investigates mechanisms contributing to short term plasticity at the calyx of Held, a giant glutamatergic synapse in the mammalian brainstem auditory system. It is a stochastic version of the model described in: Hennig, M., Postlethwaite, M., Forsythe, I.D. and Graham, B.P. (2007). A biophysical model of short-term plasticity at the calyx of Held. Neurocomputing, 70:1626-1629. This version introduces stochastic vesicle recycling and release. It has been used to investigate the information transmission properties of this synapse, as detailed in: Yang, Z., Hennig, M., Postlethwaite, M., Forsythe, I.D. and Graham, B.P. (2008). Wide-band information transmission at the calyx of Held. Neural Computation, 21(4):991-1018.
2.  MNTB Neuron: Kv3.1 currents (Wang et al 1998)
Model of Medial Nucleus of the Trapezoid Body (MNTB) neurons described in Lu-Yang Wang, Li Gan, Ian D. Forsythe and Leonard K. Kaczmarek. Contribution of the Kv3.1 potassium channel to high-frequency firing in mouse auditory neurones. J. Physiol (1998) 509.1 183-194. Created by David Kornfeld, Byram Hills High School, Armonk NY. Please email dbk1@mindspring.com for questions about the model. See Readme.txt below for more info.
3.  Modeling temperature changes in AMPAR kinetics (Postlethwaite et al 2007)
This model was used to simulate glutamatergic, AMPA receptor mediated mEPSCs (miniature EPSCs, resulting from spontaneous vesicular transmitter release) at the calyx of Held synapse. It was used to assess the influence of temperature (physiological vs. subphysiological) on the amplitude and time course of mEPSCs. In the related paper, simulation results were directly compared to the experimental data, and it was concluded that an increase of temperature accelerates AMPA receptor kinetics.
4.  Multiple mechanisms of short term plasticity at the calyx of Held (Hennig et al. 2008)
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.

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