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Sleep‐wakefulness effects after microinjections of hypocretin 1 (orexin A) in cholinoceptive areas of the cat oral pontine tegmentum
Author(s) -
MorenoBalandrán Elena,
Garzón Miguel,
Bódalo Cristina,
ReinosoSuárez Fernando,
De Andrés Isabel
Publication year - 2008
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2008.06334.x
Subject(s) - tegmentum , paramedian pontine reticular formation , wakefulness , orexin , microinjections , reticular formation , neuroscience , rapid eye movement sleep , slow wave sleep , carbachol , psychology , sleep (system call) , sleep onset , endocrinology , anesthesia , medicine , eye movement , central nervous system , midbrain , electroencephalography , stimulation , neuropeptide , receptor , psychiatry , computer science , operating system , insomnia
Hypocretinergic/orexinergic neurons, which are known to be implicated in narcolepsy, project to the pontine tegmentum areas involved in the control of rapid eye movement (REM) sleep. Here, we report the effects on sleep‐wakefulness produced by low‐volume microinjections of hypocretin (Hcrt)1 (20–30 nL, 100, 500 and 1000 μ m ) and carbachol (20–30 nL, 0.1 m ) delivered in two areas of the oral pontine tegmentum of free‐moving cats with electrodes for chronic sleep recordings: in the dorsal oral pontine tegmentum (DOPT) and in the ventral part of the oral pontine reticular nucleus (vRPO). Carbachol in the DOPT produced dissociate polygraphic states, with some but not all REM sleep signs. In contrast, carbachol in the vRPO produced a shift with short latency from wakefulness (W) to REM sleep with all of its polygraphic and behavioral signs. Hcrt‐1 in the DOPT increased W and decreased both slow‐wave sleep (SWS) and REM sleep during the first 3 h post‐drug. The same doses of Hcr‐1 in the vRPO produced a significant suppression of REM sleep without a definitive trend for changes in the other states. Both groups showed significant decreases in the number of transitions from SWS to REM sleep. Thus, Hcrt‐1 produced distinct effects in cholinoceptive areas of the oral pontine tegmentum; in the DOPT it promoted W, suppressed SWS and probably defacilitated REM sleep, and in the vRPO it directly inhibited REM sleep. Hypocretinergic/orexinergic signaling is lost in narcoleptics and this absence would mean that pontine defacilitation/inhibition of REM sleep would also be absent, explaining why these patients can fall directly into REM sleep from W.