Volume 8 Supplement 2
Information transmission by synapses with short-term synaptic plasticity
© Bibitchkov et al; licensee BioMed Central Ltd. 2007
Published: 6 July 2007
Synapses in the nervous system show dynamic behaviour in the transmission of signals from pre- to postsynaptic neuron. The postsynaptic response can decrease (short-term synaptic depression) or increase (short-term synaptic facilitation) during repeated stimulation. In this study, we formulate the theoretical description of the short-term synaptic plasticity in the calyx of Held and analyze the role of the observed dynamics for the processing of sensory information. Patch-clamp recordings of the pre- and postsynaptic elements of the calyx of Held were performed in rat brainstem slices. Experimental data suggest that the dominating dynamic property of this synapse is synaptic depression, originating from the depletion of a vesicle pool by a constant factor with subsequent recovery. The data indicate that the dynamics of recovery cannot be described on a single time scale . The synaptic dynamics can either be modelled as a process with activity-dependent recovery rate  or as originating from two releasable pools operating on different time scales .
We thank Holger Taschenberger for kindly providing the patch-clamp data. Supported by BMBF 01GQ0431.
- Sakaba T, Neher E: Calmodulin mediates rapid recruitment of fast-releasing synaptic vesicles at a calyx-type synapse. Neuron. 2001, 32 (6): 1119-1131. 10.1016/S0896-6273(01)00543-8.PubMedView ArticleGoogle Scholar
- Weis S, Schneggenburger R, Neher E: Properties of a model of Ca2+-dependent vesicle pool dynamics and short term synaptic depression. Biophys J. 1999, 77 (5): 2418-2429.PubMedPubMed CentralView ArticleGoogle Scholar
- Trommershäuser J, Schneggenburger R, Zippelius A, Neher E: Heterogeneous presynaptic release probabilities: functional relevance for short-term plasticity. Biophys J. 2003, 84 (3): 1563-1579.PubMedPubMed CentralView ArticleGoogle Scholar
This article is published under license to BioMed Central Ltd.