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Publication : Nonsynaptic communication through ATP release from volume-activated anion channels in axons.

First Author  Fields RD Year  2010
Journal  Sci Signal Volume  3
Issue  142 Pages  ra73
PubMed ID  20923934 Mgi Jnum  J:185402
Mgi Id  MGI:5428397 Doi  10.1126/scisignal.2001128
Citation  Fields RD, et al. (2010) Nonsynaptic communication through ATP release from volume-activated anion channels in axons. Sci Signal 3(142):ra73
abstractText  The release of neuronal messengers outside synapses has broad biological implications, particularly with regard to communication between axons and glia. We identify a mechanism for nonsynaptic, nonvesicular release of adenosine triphosphate (ATP) from axons through volume-activated anion channels (VAACs) activated by microscopic axon swelling during action potential firing. We used a combination of single-photon imaging of ATP release, together with imaging for intrinsic optical signals, intracellular calcium ions (Ca(2+)), time-lapse video, and confocal microscopy, to investigate action potential-induced nonsynaptic release of this neurotransmitter. ATP release from cultured embryonic dorsal root ganglion axons persisted when bafilomycin or botulinum toxin was used to block vesicular release, whereas pharmacological inhibition of VAACs or prevention of action potential-induced axon swelling inhibited ATP release and disrupted activity-dependent signaling between axons and astrocytes. This nonvesicular, nonsynaptic communication could mediate various activity-dependent interactions between axons and nervous system cells in normal conditions, development, and disease.
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