The
ethanol intake of Long-Evans male rats was recorded before, during and after deprivation of rapid eye movement (REM) sleep produced with the flowerpot technique modified by using a cuff pedestal and electrified grid floor instead of water.
Ethanol intake increased significantly during
REM-sleep deprivation. A rebound decrease in
ethanol drinking was then observed during the REM-rebound phase immediately after the termination of
REM-sleep deprivation. Because
REM-sleep deprivation has been reported to impair the function of central monoamine neuronal systems and because some studies have implicated these systems in the control of voluntary
ethanol intake, we studied whether different monoamine uptake blocking agents could antagonize the increase in
ethanol intake caused by
REM-sleep deprivation. After three days of
REM-sleep deprivation, the rats were given uptake blocking agents for
serotonin (
citalopram, 5, 10 and 20 mg/kg/day, IP),
dopamine (
GBR 12909, 5 mg/kg/day, IP) and
noradrenaline (
talsupram, 1, 5 and 10 mg/kg/day, IP).
Citalopram and
GBR 12909 did not modify the increased level of
ethanol intake, but
talsupram decreased
ethanol intake to the levels seen prior to deprivation, and during the REM-rebound phase amplified the decrease found. These effects of
talsupram could be antagonized by blocking mg/kg/day, IP).
Prazosin alone tended to increase
ethanol consumption. These findings suggest that functional alterations in central noradrenergic neurons during
REM-sleep deprivation may contribute to the concurrent increase in
ethanol intake.