Enhancement of slow-wave sleep by endotoxin and lipid A.
Some muramyl peptides derived from bacterial peptidoglycan enhance slow-wave sleep (SWS). The purpose of this study was to test whether another cell wall component, lipopolysaccharide (LPS), and its lipid A moiety also have an effect on sleep. When injected intravenously, both LPS and lipid A enhanced the duration of SWS, increased electroencephalogram delta-wave amplitudes, suppressed rapid eye movement (REM) sleep, and induced biphasic fevers. The effects of intravenously administered lipid A and LPS on SWS were present primarily during the first 3 h postinjection. Intraventricular lipid A administration enhanced SWS, did not suppress REM, and induced a monophasic fever; the SWS effect had a 3-h latency, whereas temperature started to rise during the second hour. Regardless of the route of administration, within the dose range used here, sleep was normal by the following criteria: sleep was episodic, animals could be easily aroused, and brain temperature, although elevated to "febrile" levels, continued to fluctuate during sleep-state transitions indistinguishably from control conditions. We conclude that LPS and lipid A are capable of modulating sleep.
D000818:Animals; D004305:Dose-Response Relationship, Drug; D004731:Endotoxins / Q000494:pharmacology*; D004926:Escherichia coli; D008050:Lipid A / Q000031:analogs & derivatives / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D011817:Rabbits; D012890:Sleep / Q000187:drug effects*
D004731:Endotoxins; D008050:Lipid A; D008070:Lipopolysaccharides; C049596:diphosphoryl lipid A; C048436:monophosphoryl lipid A