Adenosine mediation of presynaptic feedback inhibition of glutamate release

Dario Brambilla, David Chapman, Robert Greene

Research output: Contribution to journalArticle

44 Scopus citations

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 (τ > 10 min), consistent with the role of adenosine as a fatigue factor that inhibits the activity of cholinergic arousal centers to reduce arousal.

Original languageEnglish (US)
Pages (from-to)275-283
Number of pages9
JournalNeuron
Volume46
Issue number2
DOIs
Publication statusPublished - Apr 21 2005

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ASJC Scopus subject areas

  • Neuroscience(all)

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