Rj. Salinpascual et al., REPEATED REM-SLEEP DEPRIVATION AFTER CHRONIC HALOPERIDOL ADMINISTRATION IN THE RAT, Psychopharmacology, 131(3), 1997, pp. 216-219
Repeated haloperidol administration produces up-regulation of dopamine
(DA) receptors. REM sleep deprivation (REMSD) does also, but in addit
ion, has been shown to produce REM sleep rebound. Should DA receptor u
p-regulation play a role in REM sleep rebound, haloperidol could conce
ivably have effects similar to those observed following REMSD. This is
the central question investigated in this study.: Male Wistar rats we
re prepared for sleep recordings. They were randomly assigned to the f
ollowing groups: group 1, REMSD by small platforms (40 h REMSD + 8 h r
ecording); group 2, was the large platform control group (40 h in larg
e platforms + 8 h of recording); group 3, received 2-week daily admini
stration of haloperidol (3 mg/kg, IP) plus REMSD (40 h REMSD + 8 h of
recording); group 1, 2-week administration of haloperidol(3 mg/kg) wit
hout sleep manipulation and at the end 40 h were allowed to elapse, fo
llowing which 8 h of sleep recordings was carried out. In each group t
he sleep manipulation and/or sleep recordings were repeated five conse
cutive times. Repeated REMSD produced increases of REM sleep time afte
r each recovery in group 1. Large platforms did not produce increases
of REM sleep during the recovery trials. The 2-week administration of
haloperidol plus RER ?SD prevented REM sleep rebound (group 3). The 2-
week administration of haloperidol without sleep manipulation (group 3
) produced a REM sleep reduction. Dopamine modulation seems not to be
important for REM sleep rebound. Hypersensitivity of DA receptors deve
loped after REMSD may be an epiphenomenon associated with this sleep m
anipulation, but seems not to participate in REM sleep enhancement aft
er REMSD.