The cholinesterase inhibitor DFP facilitates the expression of paradoxical sleep (PS) propensity in rats subjected to short-term PS deprivation

• Published in: Brain research Vol. 965; no. 1; pp. 180 - 186
• Main Authors: Deurveilher, Samuel, Hennevin, Elizabeth
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 07.03.2003
• Subjects: Animals; Cholinergic transmission; Cholinesterase Inhibitors - pharmacology; Isoflurophate - pharmacology; Male; Postdeprivation REM sleep rebound; Rats; Rats, Wistar; REM sleep attempts during deprivation; REM sleep propensity; Sleep Deprivation - enzymology; Sleep Stages - physiology; Sleep, REM - drug effects; Sleep, REM - physiology; Neural basis of behaviour; REM sleep propensity; Postdeprivation REM sleep rebound; REM sleep attempts during deprivation; Cholinergic transmission
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(02)04171-9

Short-term paradoxical sleep (PS) deprivation was used to examine the effects of chronic exposure to subtoxic doses of the cholinesterase inhibitor diisopropylfluorophosphate (DFP) on PS regulation. Rats were injected once daily with DFP (0.2 mg/kg per day; s.c.) for 11 consecutive days; control rats received a daily injection of oil vehicle. The experiment was conducted on the 10th and 11th days of treatment, when brain cholinesterase inhibition induced by DFP exposure was maximal. On the 10th day, an 8-h baseline recording was carried out. On the 11th day, a 6-h PS deprivation was carried out by manually awaking rats each time they showed polygraphic signs of PS; recordings were then continued for another 2 h to examine recovery sleep. During deprivation, though they slept less than controls, DFP-treated rats made more attempts to enter PS. After deprivation, their PS rebound had an overall amount comparable to that of the controls, but its time course was shortened: whereas PS elevation was manifested through the 2 h of recovery in the control group, it occurred only during the first hour in the DFP group. These results demonstrate that chronic, low-level DFP exposure facilitated the expression of the PS propensity that accumulated as a result of PS deprivation: it enhanced the tendency for PS during deprivation; it accelerated the rate of compensatory PS expression after deprivation. They support the hypothesis that DFP promotes PS initiation by increasing cholinergic transmission.