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Volume 17, Number 7, Issue of April 1, 1997 pp. 2355-2364
Copyright ©1997 Society for Neuroscience

Adenosine Release Mediates Cyanide-Induced Suppression of CA1 Neuronal Activity

Received Nov. 16, 1996; revised Dec. 23, 1996; accepted Jan. 22, 1997.

Ping Jun Zhu and Kresimir Krnjevi

Anesthesia Research and Physiology Departments, McGill University, Montréal, Québec, Canada H3G 1Y6

The rapid suppression of CNS function produced by cyanide (CN) was studied by field, intracellular, and whole-cell recording in hippocampal slices (at 33-34°C). Population spikes and field EPSPs were depressed by 4-5 min bath applications of 50-100 µM CN (IC₅₀ was 18 µM for spikes and 72 µM for EPSPs). The actions of CN were reversibly suppressed by the adenosine antagonists 8-sulfophenyltheophylline (8-SPT; 10 µM) and 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 0.2 µM), potentiated by the adenosine transport inhibitor dipyridamole (0.5 µM), but unaffected by the K_ATP channel blocker glyburide (10 µM). Therefore the CN-induced reductions of synaptic efficacy and postsynaptic excitabilitydemonstrated by synaptic input:output plotsare mediated mainly by adenosine. In whole-cell or intracellular recordings, CN depressed EPSCs and elicited an increase in input conductance and an outward current, the reversal potential of which was approximately 90 mV (indicating that K⁺ was the major carrier). These effects also were attenuated by 8-SPT. In the presence of 1 mM Ba, CN had no significant postsynaptic action; Cs (2 mM) also prevented CN-induced outward currents but only partly blocked the increase in conductance. Another 8-SPT-sensitive action of CN was to depress hyperpolarization-activated slow inward relaxations (Q current). At room temperature (22-24°C), although it did not change holding current and slow inward relaxations, CN raised the input conductance; this effect also was prevented by 8-SPT (10 µM), but not by glyburide (10 µM). Adenosine release thus appears to be the major link between acute CN poisoning and early depression of CNS synaptic function.

Key words: adenosine antagonists; K_ATP channel blocker; synaptic transmission; outward current; input conductance; barium; cesium

This article has been cited by other articles:

				S. A. Masino and T. V. Dunwiddie Temperature-Dependent Modulation of Excitatory Transmission in Hippocampal Slices Is Mediated by Extracellular Adenosine J. Neurosci., March 15, 1999; 19(6): 1932 - 1939. [Abstract] [Full Text] [PDF]

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