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-movement (REM)-sleep homeostasis, we have administered small doses of apamin (2-5 ng), a selective blocker of the calcium-dependent SK potassium channel, injected into the lateral ventricle in rats, and characterized 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 accumulation of REM-sleep propensity is suppressed. The vast majority (84-95%) of lost REM sleep is not recovered 40 h after apamin administration. These findings suggest that accumulation of REM-sleep propensity is linked to the increased neuronal potassium conductance in nonREM sleep.
Department of Biological Sciences, Stanford University, CA 94305, USA.
J H
JH
Benington
M C
MC
Woudenberg
H C
HC
Heller
D000818:Animals; D001030:Apamin / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004566:Electrodes; D004569:Electroencephalography / Q000187:drug effects; D007276:Injections, Intraventricular; D008297:Male; D017286:Polysomnography; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012895:Sleep, REM / Q000187:drug effects*
D015221:Potassium Channels; D001030:Apamin