Alpha-adrenoceptive influences on the control of the sleep-waking cycle in the cat

Leppävuori, Antero; Putkonen, Pekka T.S.

doi:10.1016/0006-8993(80)90948-8

Cited by 71 publications

(18 citation statements)

References 44 publications

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“…In agreement with previous work in rats and cats (16,17) we found yohimbine (3 mg/kg) increased Wand decreased SWS and REMS. Administration of methoxamine in a dose ineffective by itself (4 mg/kg) to animals pretreated with yohimbine resulted in a further disruption of the sleep-wake cycle.…”

Section: Discussionsupporting

confidence: 82%

Effects of Methoxamine and a-Adrenoceptor Antagonists, Prazosin and Yohimbine, on the Sleep-Wake Cycle of the Rat

Pellejero

Monti

Baglietto

et al. 1984

Sleep

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Summary: A study was carried out on the effects of methoxamine, prazosin, and yohimbine on the sleep-wake cycle in rats prepared for chronic sleep recordings. Methoxamine (4-8 mg/kg), an al-adrenoceptor agonist, induced a doserelated increase in wakefulness (W) and a decrease in slow-wave sleep (SWS) and REM sleep (REMS). Prazosin (0.125-1 mg/kg), which selectively blocks aladrenoceptors, modified only slightly the amount of time spent in Wand SWS, and consistently decreased REMS values. Prazosin (0.5 mg/kg) reversed the effects of methoxamine, decreasing Wand increasing sleep. Yohimbine (3 mg/kg), which blocks a2-adrenoceptors, augmented Wand diminished sleep. Methoxamine (4 mg/kg) in animals pretreated with yohimbine (3 mg/kg) induced a further decrease of SWS and REMS and an increase of W Thus, pharmacological activation of al-or blocking of a2-adrenoceptors appears to decrease sleep and increase W Further, blocking of al-adrenoceptors decreases REMS. Rapid eye movement sleep depression by the aI-agonist or the aI-antagonist is tentatively ascribed to a critical change in noradrenergic transmission in the brain. Key Words:Waking-Sleep--Methoxamine-Prazosin-Yohimbine.Intraventricular administration of adrenergic agonists of al-and a2-adrenoceptors (norepinephrine, epinephrine) produces a state of prolonged wakefulness (W) (I). Compounds that indirectly activate both noradrenergic and dopaminergic receptors (amphetamine, methylphenidate) also profoundly affect the sleep-wake cycle. As a result, slow-wave sleep (SWS) and REM sleep (REMS) are decreased and W is increased (2,3). Several other compounds including methoxamine also induce an increase of waking electroencephalography (EEG), which has been related to selective activation of al-adrenoceptors (4).The present study quantifies the effect of methoxamine on the sleep-wake cycle of the rat and attempts to ascertain the role of al-and a2-receptors in the methoxamine-induced disruption of the sleep-wake cycle. The effects of methoxamine were assessed after pretreatment with either prazosin, which selectively blocks al-adrenoceptors, or yohimbine, which behaves as an antagonist of a2-adrenoceptors.

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Section: Discussionsupporting

confidence: 82%

Effects of Methoxamine and a-Adrenoceptor Antagonists, Prazosin and Yohimbine, on the Sleep-Wake Cycle of the Rat

Pellejero

Monti

Baglietto

et al. 1984

Sleep

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“…Clonidine reduces the long-term incidence of both slow-wave and r.e.m. sleep in adult cats, replacing both with a drowsy state (Leppavuori & Putkonen, 1980) The actions of idazoxan are consistent with the accepted actions of clonidine as an agonist at the same receptors. Its actions when given alone were variable in intensity, possibly reflecting varying levels of endogenous presynaptic activity.…”

Section: Discussionsupporting

confidence: 80%

“…However, the actions of clonidine on sleep are complex. In long-term studies of the effects of clonidine and other c-adrenergic agonists the incidence of all sleep states was found to be reduced (Leppavuori & Putkonen, 1980;Hilakivi, 1983), and a detailed analysis ofe.e.g. patterns after clonidine administration in rats showed that the state induced differed from any classically defined state of sleep or arousal (Pastel & Fernstrom, 1984).…”

Section: Introductionmentioning

confidence: 99%

Effects of the alpha 2‐adrenergic agonist clonidine and its antagonist idazoxan on the fetal lamb.

Bamford¹,

Dawes²,

Denny³

et al. 1986

The Journal of Physiology

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SUMMARY1. The a2-adrenergic agonist clonidine was given by aortic injection to three groups of unanaesthetized fetal lambs in utero near term. One group was intact, the second had the brain stem transacted just above the pons, and the third had bilateral section of the carotid sinus nerves and cervical vagi.2. Clonidine had similar effects in all three groups. Electrocortical activity entered a high-voltage, low-frequency episode: breathing, neck and limb movements ceased; arterial pressure remained unchanged or increased; heart rate fell or remained unchanged, and the variation in both heart rate and blood pressure was much reduced. This state lasted 10-20 min, and was followed by a period of up to 4 h during which the cycling of electrocortical activity was rapid and irregular.3. The a2-adrenergic antagonist idazoxan (0-5-2-0 mg I.A.) blocked all the actions of clonidine. When given alone it usually induced a short period of low-voltage electrocortical activity and stimulated breathing movements. These effects were present in both the intact and brain-stem-transected groups, though the stimulation of breathing was significantly reduced by brain-stem transaction. There were no consistent effects on heart rate or blood pressure.4. The effects of clonidine on fetal heart rate and electrocortical activity were similar to those described in adults, but it also had inhibitory effects, not present in adults, on fetal breathing and somatic movements.

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“…The a2-agonist clonidine inhibits LC activity [101]. In moderate doses it causes sedation, and in large doses also inhibition of NREMS and REMS [102]. a2-agonists have found clinical application as anesthetics and analgesics, especially in veterinary medicine [103].…”

Section: Neurochemistry Of Sleep and Wake Acetylcholinementioning

confidence: 99%

Neuroanatomy and neurochemistry of sleep

Stenberg

2007

Cell. Mol. Life Sci.

132

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Sleep is regulated by homeostatic and circadian factors, and the regulation of sleep of mammals shares many molecular properties with the rest state of submammalian species. Several brain structures take part in waking: the basal forebrain, posterior and lateral hypothalamus, and nuclei in the tegmentum and pons. Active sleep mechanisms are located to the preoptic/anterior hypothalamic area. In addition to acetylcholine and monoamines, glutamate and hypocretin/orexin are important waking factors. Gamma-aminobutyric acid and several peptide factors, including cytokines, growth hormone-releasing hormone and prolactin, are related to sleep promotion. Adenosine is an important homeostatic sleep factor acting in basal forebrain and preoptic areas through A1 and A2A receptors. Prolonged waking activates inducible nitric oxide synthase in the basal forebrain, which through energy depletion causes adenosine release and recovery sleep. Numerous genes have been found differentially displayed in waking compared with sleep, and they relate to neural transmission, synaptic plasticity, energy metabolism and stress protection. The genetic background of a few sleep disorders has been solved.

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Alpha-adrenoceptive influences on the control of the sleep-waking cycle in the cat

Cited by 71 publications

References 44 publications

Effects of Methoxamine and a-Adrenoceptor Antagonists, Prazosin and Yohimbine, on the Sleep-Wake Cycle of the Rat

Effects of Methoxamine and a-Adrenoceptor Antagonists, Prazosin and Yohimbine, on the Sleep-Wake Cycle of the Rat

Effects of the alpha 2‐adrenergic agonist clonidine and its antagonist idazoxan on the fetal lamb.

Neuroanatomy and neurochemistry of sleep

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