Oxygen-glucose deprivation induces ATP release via maxi-anion channels in astrocytes
Pannexin
Connexon
DOI:
10.1007/s11302-007-9077-8
Publication Date:
2007-09-11T13:28:13Z
AUTHORS (3)
ABSTRACT
ATP represents a major gliotransmitter that serves as signaling molecule for the cross talk between glial and neuronal cells. has been shown to be released by astrocytes in response number of stimuli under nonischemic conditions. In this study, using luciferin-luciferase assay, we found mouse primary culture also exhibit massive release ischemic stress mimicked oxygen-glucose deprivation (OGD). Using biosensor technique, local concentration at surface single was increase around 4 muM. The OGD-induced inhibited Gd(3+) arachidonic acid but not blockers volume-sensitive outwardly rectifying Cl(-) channels, cystic fibrosis transmembrane conductance regulator (CFTR), multidrug resistance-related protein (MRP), connexin or pannexin hemichannels, P2X(7) receptors, exocytotic vesicular transport. cell-attached patches on astrocytes, OGD caused activation maxi-anion channels were sensitive acid. channel permeable ATP(4-) with permeability ratio P(ATP)/P(Cl) = 0.11. Thus, it is concluded induces from may serve ATP-releasing pathway
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