APAMIN, A SELECTIVE SK POTASSIUM CHANNEL BLOCKER, SUPPRESSES REM-SLEEP WITHOUT A COMPENSATORY REBOUND

To determine the role of neuronal potassium conductance in rapid-eye-m ovement (REM)-sleep homeostasis, we have administered small doses of a pamin (2-5 ng), a selective blocker of the calcium-dependent SK potass ium channel, injected into the lateral ventricle in rats, and characte rized the resultant effects on REM-sleep expression. Apamin produces a dose-dependent reduction in REM-sleep expression without an increase in the frequency of attempts to enter REM sleep, suggesting that accum ulation of REM-sleep propensity is suppressed. The vast majority (84-9 5%) of lost REM sleep is not recovered 40 h after apamin administratio n. These findings suggest that accumulation of REM-sleep propensity is linked to the increased neuronal potassium conductance in nonREM slee p.