The presence of ethanol, 100 mM, in the superfusate enhanced the spontaneous release of previously uptaken [3H]-dopamine from slices of rat corpus striatum, but produced a small inhibition of K+-stimulated release. The concomitant presence of picrotoxin, 10 μM, in the superfusate prevented the enhancement of spontaneous release of [3H]-doamine by ethanol with equivocal effects on K+-stimulated release. When present in the superfusate alone picrotoxin had no effect on [3H]-dopamine release. Considerable circumstantial evidence links some actions of ethanol with an interaction with the chloride ionophore. Thus, picrotoxin (Leitch, Backes, Siegman and Guthrie, 1977) can overcome the behavioural depressant action of ethanol and the enhancement of benzodiazepine binding induced by 100 mM ethanol (Davis and Ticku, 1981) is almost completely reversed by 10 μM picrotoxin. Here we report that a neurochemical effect of ethanol, that of increasing the spontaneous release of [3H]-dopamine, is also inhibited by picrotoxin. It should be noted that, although high concentrations of GABA can also enhance [3H]-dopamine release in this system, this effect of GABA is probably mediated by GABA uptake into neuronal terminals and is not modified by picrotoxin (Reimann, Zumstein and Starke, 1982).
|Number of pages||3|
|Issue number||12 PART 2|
|State||Published - Dec 1983|
Bibliographical noteFunding Information:
This work was supported by the Medical Council on Alcoholism.
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience