O'Regan M H, Phillis J W
Department of Physiology, School of Medicine, Wayne State University, Detroit, MI 48201.
Brain Res. 1988 Apr 5;445(2):376-9. doi: 10.1016/0006-8993(88)91203-6.
The triazolobenzodiazepine triazolam, applied iontophoretically onto rat cerebral cortical neurons, potentiated the magnitude and duration of adenosine-elicited depressions of spontaneous activity. Triazolam did not enhance the depressions evoked by adenosine 5'-N-ethylcarboxamide, an uptake resistant analog of adenosine, suggesting that potentiation of adenosine resulted from an inhibition of adenosine uptake. With larger application currents, triazolam depressed the firing of cortical neurons. This action was blocked by the adenosine antagonist caffeine (20 mg/kg, i.v.) implying that the depression resulted from an accumulation of endogenously released adenosine.