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Below are two excellent papers that outline the mechanism by which astrocytes regulate synaptic strength. The first one shows the most important pathway, I think. Here's my summary of the story from the first paper:
1) ATP released locally by local activity (either from the granule neurons or neighboring astrocytes)
2) P2Y1 receptors bind ATP, initiating Ca influx in the perisynaptic compartment of the astrocyte
3) Ca influx triggers glutamate release (fyi, astrocytes have glutamate vesicles primed at the tripartate synapse).
4) glutamate from astrocytes binds to the NR2B subunit on the NMDA receptors on the pre-synaptic cell
5) NR2B binding increases the frequency of mESPCs, potentiating the post-synaptic cell, bringing it closer to threshold.
Note: astrocytes are connected to each other in gap-junction networks. It would be interesting to see what kind of influences they have on each other with respect to perisynaptic glutamate release. The paper shows how Ca diffuses through the astrocyte network via these gap junctions, but it just mentions it in passing, more-or-less.
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Glutamate exocytosis from astrocytes controls synaptic strength
Pascal Jourdain, et al. Nature Neuroscience 10, 331 - 339 (2007)
Published online: 18 February 2007 | doi:10.1038/nn1849
http://www.ncbi.nlm.nih.gov/pubmed/17310248 (pubmed entry)
http://www.nature.com/neuro/journal/v10/n3/full/nn1849.html (paper)
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Plasmalemmal Na+/Ca2+ exchanger modulates Ca 2+ -dependent exocytotic release of glutamate from rat cortical astrocytes.
Reno C Reyes, et al. ASN NEURO 4(1)
e00075.doi:10.1042/AN20110059
http://www.asnneuro.org/an/004/e075/004e075.pdf[/URL] (paper)
1) ATP released locally by local activity (either from the granule neurons or neighboring astrocytes)
2) P2Y1 receptors bind ATP, initiating Ca influx in the perisynaptic compartment of the astrocyte
3) Ca influx triggers glutamate release (fyi, astrocytes have glutamate vesicles primed at the tripartate synapse).
4) glutamate from astrocytes binds to the NR2B subunit on the NMDA receptors on the pre-synaptic cell
5) NR2B binding increases the frequency of mESPCs, potentiating the post-synaptic cell, bringing it closer to threshold.
Note: astrocytes are connected to each other in gap-junction networks. It would be interesting to see what kind of influences they have on each other with respect to perisynaptic glutamate release. The paper shows how Ca diffuses through the astrocyte network via these gap junctions, but it just mentions it in passing, more-or-less.
--------------------------------------------------------
Glutamate exocytosis from astrocytes controls synaptic strength
Pascal Jourdain, et al. Nature Neuroscience 10, 331 - 339 (2007)
Published online: 18 February 2007 | doi:10.1038/nn1849
http://www.ncbi.nlm.nih.gov/pubmed/17310248 (pubmed entry)
http://www.nature.com/neuro/journal/v10/n3/full/nn1849.html (paper)
----------------------------------------------------------
Plasmalemmal Na+/Ca2+ exchanger modulates Ca 2+ -dependent exocytotic release of glutamate from rat cortical astrocytes.
Reno C Reyes, et al. ASN NEURO 4(1)
e00075.doi:10.1042/AN20110059http://www.asnneuro.org/an/004/e075/004e075.pdf[/URL] (paper)
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