ArticleBMC neuroscience2011
Astrocyte-mediated short-term synaptic depression in the rat hippocampal CA1 area: two modes of decreasing release probability.
Article in BMC neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Combinatorial gene therapy for epilepsy: Gene sequence positioning and AAV serotype influence expression and inhibitory effect on seizures.Gene therapy · 2023Article
- Electrophysiology of Endocannabinoid Signaling.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Astrocytic Endocannabinoids Mediate Hippocampal Transient Heterosynaptic Depression.Neurochemical research · 2020Article
- The Small and Dynamic Pre-primed Pool at the Release Site; A Useful Concept to Understand Release Probability and Short-Term Synaptic Plasticity?Frontiers in synaptic neuroscience · 2019Review
- Postactivation depression of the Ia EPSP in motoneurons is reduced in both the G127X SOD1 model of amyotrophic lateral sclerosis and in aged mice.Journal of neurophysiology · 2015Article
- Bursting reverberation as a multiscale neuronal network process driven by synaptic depression-facilitation.PloS one · 2015Article
- Computational quest for understanding the role of astrocyte signaling in synaptic transmission and plasticity.Frontiers in computational neuroscience · 2012Article
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2 authors.
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Abstract
backgroundSynaptic burst activation feeds back as a short-term depression of release probability at hippocampal CA3-CA1 synapses. This short-term synaptic plasticity requires functional astrocytes and it affects both the recently active (< 1 s) synapses (post-burst depression) as well as inactive neighboring synapses (transient heterosynaptic depression). The aim of this study was to investigate and compare the components contributing to the depression of release probability in these two different scenarios.
resultsWhen tested using paired-pulses, following a period of inactivity, the transient heterosynaptic depression was expressed as a reduction in the response to only the first pulse, whereas the response to the second pulse was unaffected. This selective depression of only the first response in a high-frequency burst was shared by the homosynaptic post-burst depression, but it was partially counteracted by augmentation at these recently active synapses. In addition, the expression of the homosynaptic post-burst depression included an astrocyte-mediated reduction of the pool of release-ready primed vesicles.
conclusionsOur results suggest that activated astrocytes depress the release probability via two different mechanisms; by depression of vesicular release probability only at inactive synapses and by imposing a delay in the recovery of the primed pool of vesicles following depletion. These mechanisms restrict the expression of the astrocyte-mediated depression to temporal windows that are typical for synaptic burst activity.
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