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Volume‐regulated anion channels do not contribute extracellular adenosine during the hypoxic depression of excitatory synaptic transmission in area CA1 of rat hippocampus
Author(s) -
Pearson Tim,
Frenguelli Bruno G.
Publication year - 2000
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2000.00201.x
Subject(s) - adenosine , extracellular , excitatory postsynaptic potential , hypoxia (environmental) , neurotransmission , adenosine a1 receptor , chemistry , antagonist , adenosine receptor , medicine , endocrinology , neuroscience , pharmacology , biology , receptor , biochemistry , agonist , organic chemistry , oxygen
We investigated whether volume‐regulated anion channels (VRACs) contributed to the accumulation of extracellular adenosine during hypoxia in area CA1. The rapid hypoxic depression of the fEPSP was greatly attenuated by the selective adenosine A 1 receptor antagonist DPCPX (50 n m ), but not affected by the VRAC blockers tamoxifen (10–30 μ m ) or DNDS (1 m m ). Our data argue against the efflux of adenosine per se or its precursor ATP through VRACs as making a significant contribution to extracellular adenosine during the early stages of hypoxia.