Advanced

Astrocyte-mediated short-term synaptic depression in the rat hippocampal CA1 area : two modes of decreasing release probability

Andersson, My LU and Hanse, Eric (2011) In BMC Neuroscience 12.
Abstract

BACKGROUND: Synaptic 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.

RESULTS: When 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... (More)

BACKGROUND: Synaptic 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.

RESULTS: When 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.

CONCLUSIONS: Our 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.

(Less)
Please use this url to cite or link to this publication:
author
publishing date
type
Contribution to journal
publication status
published
keywords
Animals, Astrocytes, Cells, Cultured, Computer Simulation, Cortical Spreading Depression, Hippocampus, Models, Neurological, Models, Statistical, Rats, Rats, Wistar, Synaptic Transmission, Journal Article, Research Support, Non-U.S. Gov't
in
BMC Neuroscience
volume
12
publisher
BioMed Central
external identifiers
  • scopus:80052024949
ISSN
1471-2202
DOI
10.1186/1471-2202-12-87
language
English
LU publication?
no
id
b41a6b78-d2fb-4454-b76d-7386bafdbc97
date added to LUP
2017-03-30 16:56:55
date last changed
2017-04-02 04:36:30
@article{b41a6b78-d2fb-4454-b76d-7386bafdbc97,
  abstract     = {<p>BACKGROUND: Synaptic 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 (&lt; 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.</p><p>RESULTS: When 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.</p><p>CONCLUSIONS: Our 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.</p>},
  articleno    = {87},
  author       = {Andersson, My and Hanse, Eric},
  issn         = {1471-2202},
  keyword      = {Animals,Astrocytes,Cells, Cultured,Computer Simulation,Cortical Spreading Depression,Hippocampus,Models, Neurological,Models, Statistical,Rats,Rats, Wistar,Synaptic Transmission,Journal Article,Research Support, Non-U.S. Gov't},
  language     = {eng},
  month        = {08},
  publisher    = {BioMed Central},
  series       = {BMC Neuroscience},
  title        = {Astrocyte-mediated short-term synaptic depression in the rat hippocampal CA1 area : two modes of decreasing release probability},
  url          = {http://dx.doi.org/10.1186/1471-2202-12-87},
  volume       = {12},
  year         = {2011},
}