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Updated: Aug 18, 2026

Presynaptically Silent Synapses Studied with Light Microscopy
Published on: January 4, 2010
Adenosine mediation of presynaptic feedback inhibition of glutamate release
Dario Brambilla1, David Chapman, Robert Greene
1Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Abstract:
Conditions of increased metabolic demand relative to metabolite availability are associated with increased extracellular adenosine in CNS tissue. Synaptic activation of postsynaptic NMDA receptors on neurons of the cholinergic brainstem arousal center can increase sufficient extracellular adenosine to act on presynaptic A1 adenosine receptors (A1ADRs) of glutamate terminals, reducing release from the readily releasable pool. The time course of the adenosine response to an increase in glutamate release is slow (tau > 10 min), consistent with the role of adenosine as a fatigue factor that inhibits the activity of cholinergic arousal centers to reduce arousal.
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