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J Neurophysiol (February 15, 2006). doi:10.1152/jn.00694.2005
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Submitted on July 1, 2005
Accepted on February 10, 2006

Endogenous activation of adenosine A1 receptors but not P2X receptors during high frequency synaptic transmission at the calyx of Held

Adrian Y. C. Wong1, Brian Billups1, Jamie Johnston1, Richard J. Evans1, and Ian D. Forsythe1*

1 MRC Toxicology Unit, University of Leicester, Leicester, Leicestershire, United Kingdom

* To whom correspondence should be addressed. E-mail: idf{at}le.ac.uk.

Activation of presynaptic receptors plays an important role in modulation of transmission at many synapses, particularly during high frequency trains of stimulation. Adenosine-triphosphate (ATP) is co-released with several neurotransmitters and acts at presynaptic sites to reduce transmitter release; such presynaptic P2X receptors occur at inhibitory and excitatory terminals in the medial nucleus of the trapezoid body (MNTB). We have investigated the mechanism of purinergic modulation during high frequency repetitive stimulation at the calyx of Held synapse. Suppression of calyceal EPSCs by ATP and ATP{gamma}S (100 µM) was mimicked by adenosine application and was blocked by DPCPX (10 µM), indicating mediation by adenosine A1 receptors. DPCPX enhanced EPSC amplitudes during high frequency synaptic stimulation, suggesting that adenosine has a physiological role in modulating transmission at the calyx. The Luciferin/Luciferase method was used to probe for endogenous ATP release (at 37°C), but no release was detected. Blockers of ecto-nucleotidases also had no effect on endogenous synaptic depression, suggesting that it is adenosine acting on A1 receptors, rather than degradation of released ATP, which accounts for presynaptic purinergic suppression of synaptic transmission during physiological stimulus trains at this glutamatergic synapse.




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