Mechanisms of glutamate release from astrocytes: gap junction "hemichannels", purinergic receptors and exocytotic release.
Neuronal exocytotic release of glutamate at synapses involves a highly specialized vesicular apparatus, consisting of a variety of proteins connected to the vesicles or required for vesicular fusion to the presynaptic membrane. Astrocytes also release glutamate, and recent evidence indicates that this release can modify neuronal function. Several mechanisms have been proposed for astrocytic release of glutamate under pathological conditions, such as reversal of glutamate transporters and opening of volume sensitive ion channels. In this review we limit our discussion to findings supporting the exocytotic release of glutamate, as well as two new pathways implicated in this release, the ionotropic (P2X) purinergic receptors and gap junction hemichannels.
Parpura
Vladimir
V
Department of Cell Biology and Neuroscience, Center for Nanoscale Science and Engineering, University of California, Riverside, CA 92521, USA. vladimir.parpura@ucr.edu
Scemes
Eliana
E
Spray
David C
DC
D000818:Animals; D001253:Astrocytes / Q000502:physiology*; D002118:Calcium / Q000502:physiology; D005089:Exocytosis / Q000502:physiology*; D017629:Gap Junctions / Q000502:physiology*; D018698:Glutamic Acid / Q000378:metabolism*; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000502:physiology; D011983:Receptors, Purinergic / Q000502:physiology*
D007473:Ion Channels; D009419:Nerve Tissue Proteins; D011983:Receptors, Purinergic; D018698:Glutamic Acid; D002118:Calcium