We have examined the effect of adenosine on the membrane properties of cultured embryonic mouse striatal neurons using patch electrode techniques. Adenosine at 50μM effectively blocked spontaneous action potential activity. Adenosine or 2-chloroadenosine caused a slow hyperpolarization of the membrane potential and, under voltage clamp, an outward current that was blocked by 1 mM theophylline. ATP also caused a hyperpolarization that was slower and weaker than the adenosine response and could be blocked by 1 mM theophylline. The current induced by adenosine appears to be carried by potassium since an inward current was generated by adenosine when the cells were internally perfused with cesium salts and the reversal potential of the outward current shifted 57 mV with a 10-fold change in extracellular potassium concentration. The adenosine response is voltage dependent in that the current evoked by adenosine is reduced at holding potentials more positive than -55 mV, despite a larger driving force. Though calcium influx is not required for adenosine to activate the potassium conductance, some components of the cytosol may be essential, since the response is lost during intracellular perfusion.
|Original language||English (US)|
|Number of pages||5|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|State||Published - Jan 1 1985|
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