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First published online on March 15, 2002.
 Copyright © 2002 by The Physiological Society
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2001.013193v1
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Received August 24, 2001
Accepted after revision February 1, 2002

Spike-independent release of ATP from Xenopus spinal neurons evoked by activation of glutamate receptors

Paul Brown1 and Nicholas Dale1*

1 Department of Biological Sciences, University of Warwick, Coventry CV4 7AL, UK

* To whom correspondence should be addressed. E-mail: n.e.dale{at}warwick.ac.uk.

As the release of ATP from neurons has only been directly studied in a few cases, we have used patch sniffing to examine ATP release from Xenopus spinal neurons. ATP release was detected following intracellular current injection to evoke spikes. However, spiking was not essential as both glutamate and NMDA could evoke release of ATP in the presence of TTX. Neither acetylcholine nor high K+ was effective at inducing ATP release in the presence of TTX. Although Cd2+ blocked glutamate-evoked release of ATP suggesting a dependence on Ca2+ entry, neither {omega}-conotoxin-GVIA nor nifedipine prevented ATP release. N-type and L-type channels are thus not essential for glutamate-evoked ATP release. That glutamate receptors can elicit release in the absence of spiking suggests a close physical relationship between these receptors, the Ca2+ channels and release sites. As the dependence of ATP release on the influx of Ca2+ through Ca2+ channel subtypes differs from that of synaptic transmitter release, ATP may be released from sites that are distinct from those of the principal transmitter. In addition to its role as a fast transmitter, ATP may thus be released as a consequence of the activation of excitatory glutamatergic synapses and act to signal information about activity patterns in the nervous system.




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