Fig 1.

Ethanol dose-dependently inhibits in vitro glutamate-induced phase shifts. A. Shown are the 2 h means ± SEM of SCN neuronal activity from several experiments. Under control (no treatment) conditions, neuronal activity peaks near ZT 6 on the second day in vitro. Neuronal activity peaks approximately 3 h later than normal after brain slices are treated with glutamate (1mM) at ZT 16, indicating the SCN clock has been phase-delayed by 3 h. Co-application of 20mM ethanol treatment with glutamate blocks the phase delay. Glutamate treatment alone at ZT 23 advances the time of peak activity by about 3 hr, and again, this is prevented by co-treatment with 20 mM EtOH. Horizontal bars: time of lights-off in the animal colony; vertical bars: time of drug treatment; dotted line: mean time-of-peak in control experiments. B. Dose response curve for ethanol inhibition of glutamate-induced phase delays. Shown are the mean phase delays (±SEM) induced by 1 mM glutamate applied alone or co-applied with EtOH at ZT 16.