Effects of Opioid Microinjections in the Nucleus of the Solitary Tract on the Sleep-Wakefulness Cycle States in Cats

Reinoso-Barbero, Francisco; Andrés, Isabel de

doi:10.1097/00000542-199501000-00019

Cited by 50 publications

(21 citation statements)

References 42 publications

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“…Administration of morphine through veins and heart ventricles has been found to increase NREM sleep in beagles (Pickworth et al, 1982). The microinjection of morphine into the noradrenergic locus coeruleus (LC) or nucleus of the solitary was found to increase SWS in cats (Garzon et al, 1995;Reinoso-Barbero and de Andres, 1995). In in vitro mouse brain slices, morphine has been shown to inhibit the orexin arousal system (Li and van den Pol, 2008).…”

Section: Discussionmentioning

confidence: 99%

Morphine Inhibits Sleep-Promoting Neurons in the Ventrolateral Preoptic Area Via Mu Receptors and Induces Wakefulness in Rats

Wang

Yue

et al. 2012

Neuropsychopharmacol

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Morphine is the most efficacious and widely prescribed treatment for pain. However, it decreases the total amount of deep sleep and rapid eye movement sleep in humans. Acute morphine administration at low doses causes wakefulness in animal models. To clarify the mechanism by which morphine affects sleep-wake behavior, we investigated the effects of morphine on the sleep-promoting neurons of the ventrolateral preoptic area (VLPO), a putative sleep-active nucleus, using in vitro brain slices by the patch-clamp technique. We also examined the effects of morphine on sleep-wake profiles after administration of opioid receptor antagonist to the VLPO using EEG and electromyogram recordings in freely moving rats. The results showed that morphine inhibited the firing rate of sleep-promoting neurons and hyperpolarized their membrane potentials without affecting interneurons in the VLPO. Morphine-induced hyperpolarization of membrane potentials could be reversed by, D-Phe-Cys-Thr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP), a mu receptor antagonist, in the presence of tetrodotoxin. However, after the mu receptors were blocked by CTOP, morphine still suppressed the firing of the sleep-promoting neurons. This effect was antagonized by nor-BIN, a kappa receptor antagonist. Activation of kappa receptor by U50488H inhibited the firing of the sleep-promoting neurons. These results indicate that morphine could inhibit the activity of sleep-promoting neurons in the VLPO through mu and kappa receptors. EEG recordings revealed that morphine injected subcutaneously induced arousal in a dose-dependent manner. CTOP microinjected into VLPO antagonized the arousal effects of morphine, but nor-BIN did not. However, CTOP alone was not associated with any changes in the physiological sleep-wake cycle. Taken together, these findings clearly indicate that morphine inhibits sleep-promoting neurons in the VLPO by affecting mu receptors and so induces wakefulness in rats.

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Section: Discussionmentioning

confidence: 99%

Morphine Inhibits Sleep-Promoting Neurons in the Ventrolateral Preoptic Area Via Mu Receptors and Induces Wakefulness in Rats

Wang

Yue

et al. 2012

Neuropsychopharmacol

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“…Although the reduction was much larger in the Combined group, the Balanced anaesthesia using opiates also reduced the minimal alveolar concentration (MAC) for inhalatory agents [13]. Hypnotic and electroencephalographic effects after opiate administration were identified long ago [14] and even the neural basis for the hypnotic effect of opiates has been elucidated [15]. However, the BIS monitoring algorithm does not seem to adequately reflect the electroencephalographic effect of opiates [16].…”

Section: Discussionmentioning

confidence: 99%

The effect of epidural bupivacaine on maintenance requirements of sevoflurane evaluated by bispectral index in children

Reinoso-Barbero¹,

Martinez-Garcia²,

Hernández-Gancedo³

et al. 2006

European Journal of Anaesthesiology

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“…When this system is disconnected from the forebrain by a midpontine pretrigeminal transection, a long-lasting arousal, both in behavior and electroencephalogram (EEG) in cats is the result. The most caudal region located within the medulla, which is implicated in the regulation of slow wave sleep, is the nucleus of the solitary tract (Eguchi & Satoh, 1980;Reinoso-Barbero and de Andrés, 1995). In this area a population of neurons is maximally active when slow wave sleep occurs (Siegel, 1990).…”

Section: Neuroanatomical Structuresmentioning

confidence: 99%

Neuronal Phenomena Associated with Vigilance and Consciousness: From Cellular Mechanisms to Electroencephalographic Patterns

Coenen

1998

Consciousness and Cognition

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Effects of Opioid Microinjections in the Nucleus of the Solitary Tract on the Sleep-Wakefulness Cycle States in Cats

Abstract: These results indicate that endogenous opioids could be involved in controlling electrocortical activity generated by NST and that activation of mu and delta NST opioid receptors enhanced the electroencephalographic synchronization associated with behavioral slow wave sleep in cats.

Cited by 50 publications

References 42 publications

Morphine Inhibits Sleep-Promoting Neurons in the Ventrolateral Preoptic Area Via Mu Receptors and Induces Wakefulness in Rats

Morphine Inhibits Sleep-Promoting Neurons in the Ventrolateral Preoptic Area Via Mu Receptors and Induces Wakefulness in Rats

The effect of epidural bupivacaine on maintenance requirements of sevoflurane evaluated by bispectral index in children

Neuronal Phenomena Associated with Vigilance and Consciousness: From Cellular Mechanisms to Electroencephalographic Patterns

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