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The Journal of Neuroscience, April 15, 1999, 19(8):3204-3212
Key Role of 5-HT1B Receptors in the Regulation of
Paradoxical Sleep as Evidenced in 5-HT1B Knock-Out Mice
Benjamin
Boutrel1,
Bernard
Franc1,
René
Hen2,
Michel
Hamon1, and
Joëlle
Adrien1
1 Institut National de la Santé et de la
Recherche Médicale U288, NeuroPsychoPharmacologie
Moléculaire, Cellulaire et Fonctionnelle, 75634 Paris Cedex 13, France, and 2 Center for Neurobiology and Behavior,
Columbia University, New York, New York 10032
The involvement of 5-HT1B receptors in the regulation
of vigilance states was assessed by investigating the spontaneous
sleep-waking cycles and the effects of 5-HT receptor ligands on sleep
in knock-out (5-HT1B /) mice that do not express this
receptor type. Both 5-HT1B/ and wild-type 129/Sv mice
exhibited a clear-cut diurnal sleep-wakefulness rhythm, but knock-out
animals were characterized by higher amounts of paradoxical sleep and
lower amounts of slow-wave sleep during the light phase and by a lack
of paradoxical sleep rebound after deprivation. In wild-type mice, the
5-HT1B agonists CP 94253 (1-10 mg/kg, i.p.) and RU
24969 (0.25-2.0 mg/kg, i.p.) induced a dose-dependent reduction of
paradoxical sleep during the 2-6 hr after injection, whereas the
5-HT1B/1D antagonist GR 127935 (0.1-1.0 mg/kg, i.p.)
enhanced paradoxical sleep. In addition, pretreatment with GR 127935, but not with the 5-HT1A antagonist WAY 100635, prevented
the effects of both 5-HT1B agonists. In contrast, none of
the 5-HT1B receptor ligands, at the same doses as those
used in wild-type mice, had any effect on sleep in
5-HT1B/ mutants. Finally, the 5-HT1A
agonist 8-OH-DPAT (0.2-1.2 mg/kg, s.c.) induced in both strains a
reduction in the amount of paradoxical sleep. Altogether, these data
indicate that 5-HT1B receptors participate in the
regulation of paradoxical sleep in the mouse.
Key words:
serotonin; 5-HT1B receptor; paradoxical
sleep; knock-out; mice
Copyright © 1999 Society for Neuroscience 0270-6474/99/1983204-09$05.00/0
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