Compounds > 4-4--dinitro-2-2--stilbenedisulfonic-acid

4-4--dinitro-2-2--stilbenedisulfonic-acid and 1-3-dipropyl-8-cyclopentylxanthine

4-4--dinitro-2-2--stilbenedisulfonic-acid has been researched along with 1-3-dipropyl-8-cyclopentylxanthine* in 1 studies

Other Studies

1 other study(ies) available for 4-4--dinitro-2-2--stilbenedisulfonic-acid and 1-3-dipropyl-8-cyclopentylxanthine

Article	Year
Volume-regulated anion channels do not contribute extracellular adenosine during the hypoxic depression of excitatory synaptic transmission in area CA1 of rat hippocampus. The European journal of neuroscience, 2000, Volume: 12, Issue:8 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 A1 receptor antagonist DPCPX (50 nM), but not affected by the VRAC blockers tamoxifen (10-30 microM) or DNDS (1 mM). 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. Topics: Adenosine; Adenosine Triphosphate; Animals; Anions; Estrogen Antagonists; Excitatory Postsynaptic Potentials; Female; Hippocampus; Hypoxia, Brain; In Vitro Techniques; Male; Purinergic P1 Receptor Antagonists; Rats; Rats, Sprague-Dawley; Receptors, Purinergic P1; Stilbenes; Synaptic Transmission; Tamoxifen; Xanthines	2000

Article

Year

Volume-regulated anion channels do not contribute extracellular adenosine during the hypoxic depression of excitatory synaptic transmission in area CA1 of rat hippocampus.

The European journal of neuroscience, 2000, Volume: 12, Issue:8

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 A1 receptor antagonist DPCPX (50 nM), but not affected by the VRAC blockers tamoxifen (10-30 microM) or DNDS (1 mM). 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.

Topics: Adenosine; Adenosine Triphosphate; Animals; Anions; Estrogen Antagonists; Excitatory Postsynaptic Potentials; Female; Hippocampus; Hypoxia, Brain; In Vitro Techniques; Male; Purinergic P1 Receptor Antagonists; Rats; Rats, Sprague-Dawley; Receptors, Purinergic P1; Stilbenes; Synaptic Transmission; Tamoxifen; Xanthines

2000