What is it about?
We found that astrocytes restrict depolarization- and glucocorticoid-induced endocannabinoid (2-AG) actions to glutamate synapses. Evoked endocannabinoid suppression of GABA release was seen only after blocking glial metabolism with fluorocitrate or after glial retraction induced by dehydration, suggesting that astrocytes control evoked endocannabinoid spillover onto GABA synapses. Interestingly, we found that AEA tonically suppresses GABA release, which is not regulated by glial coverage.
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Why is it important?
This is the first demonstration of endocannabinoid (2-AG) spillover between glutamate and GABA synapses that is controlled by astrocytes. It suggests that 2-AG access to presynaptic CB1 receptors is subject to regulation by astrocytes, but AEA access is not. This, in turn, suggests that the two endocannabinoids are transported to presynaptic receptors using different mechanisms.
Perspectives
This finding is exciting because it suggests that 2-AG diffuses in the extracellular space, presumably carried by a water soluble transporter, whereas AEA is transported via a different mechanism that does not use extracellular diffusion.
Professor Jeffrey G Tasker
Tulane University
Read the Original
This page is a summary of: Glial Control of Endocannabinoid Heterosynaptic Modulation in Hypothalamic Magnocellular Neuroendocrine Cells, Journal of Neuroscience, November 2013, Society for Neuroscience,
DOI: 10.1523/jneurosci.2971-12.2013.
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