Modulation of morphine-induced EEG and behavioral effects by dynorphin A-(1-13) in non-tolerant and morphine-tolerant rats

Hong, O.; Young, Gerald A.; Khazan, N.

doi:10.1016/0028-3908(88)90095-0

Cited by 16 publications

(3 citation statements)

References 20 publications

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“…As these patients usually received a high dose of morphine for analgesia, morphine increased sleep in patients with pain may be only a rebound of sleep after pain-induced insomnia, which is referred to patients' pain relieving. In rats, cats, and dogs, after injection of morphine at high doses there was a dissociation of EEG and behavior, where bursts of high-voltage waves were seen over a background of desynchrony; meanwhile the animal was quiet and showed behavioral stupor (Hong et al, 1988;Tortella et al, 1978;de Andres et al, 1984;Pickworth and Sharpe, 1979). Administration of morphine through veins and heart ventricles has been found to increase NREM sleep in beagles (Pickworth et al, 1982).…”

Section: Discussionmentioning

confidence: 95%

“…Electrophysiological study revealed that morphine excites the histaminergic arousal system in rats (Eriksson et al, 2000). However, morphine particularly at high doses had a strong sedative effect in human and animals (Hong et al, 1988;Tortella et al, 1978;de Andres et al, 1984;Pickworth and Sharpe, 1979;Matejcek et al, 1988). In humans, morphine at high doses improved sleep in patients with comorbid pain (Adams et al, 2006;Paqueron et al, 2002;Rosenthal et al, 2007).…”

Section: Discussionmentioning

confidence: 95%

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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: 95%

Section: Discussionmentioning

confidence: 95%

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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“…The role of the Dyn / KOR system in modulating these emergent properties is still unknown. While the Dyn / KOR system has been shown to regulate oscillations in EEG signals in humans and animal models [ 44 – 47 ], it is unclear how much these alterations reflect modulation of oscillations and entrainment of single cell encoding within mPFC circuits. The KOR agonist, Salvinorin A, triggers robust changes in “functional connectivity” across broad cortical networks as assessed by fMRI [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

Dynorphin / kappa-opioid receptor regulation of excitation-inhibition balance toggles afferent control of prefrontal cortical circuits in a pathway-specific manner

Yarur,

Casello,

Tsai

et al. 2023

Mol Psychiatry

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The medial prefrontal cortex (mPFC) controls behavior via connections with limbic excitatory afferents that engage various inhibitory motifs to shape mPFC circuit function. The dynorphin (Dyn) / kappa-opioid receptor (KOR) system is highly enriched in the mPFC, and its dysregulation is implicated in neuropsychiatric disorders. However, it is unclear how the Dyn / KOR system modulates excitatory and inhibitory circuits that are integral for mPFC information processing and behavioral control. Here, we provide a circuit-based framework wherein mPFC Dyn / KOR signaling regulates excitation-inhibition balance by toggling which afferents drive mPFC neurons. Dyn / KOR regulation of afferent inputs is pathway-specific. Dyn acting on presynaptic KORs inhibits glutamate release from afferent inputs to the mPFC, including the basolateral amygdala (BLA), paraventricular nucleus of the thalamus, and contralateral cortex. The majority of excitatory synapses to mPFC neurons, including those from the ventral hippocampus (VH), do not express presynaptic KOR, rendering them insensitive to Dyn / KOR modulation. Dyn / KOR signaling also suppresses afferent-driven recruitment of specific inhibitory sub-networks, providing a basis for Dyn to disinhibit mPFC circuits. Specifically, Dyn / KOR signaling preferentially suppresses SST interneuron- relative to PV interneuron-mediated inhibition. Selective KOR action on afferents or within mPFC microcircuits gates how distinct limbic inputs drive spiking in mPFC neurons. Presynaptic Dyn / KOR signaling decreases KOR-positive input-driven (e.g. BLA) spiking of mPFC neurons. In contrast, KOR-negative input recruitment of mPFC neurons is enhanced by Dyn / KOR signaling via suppression of mPFC inhibitory microcircuits. Thus, by acting on distinct circuit elements, Dyn / KOR signaling shifts KOR-positive and negative afferent control of mPFC circuits, providing mechanistic insights into the role of neuropeptides in shaping mPFC function. Together, these findings highlight the utility of targeting the mPFC Dyn / KOR system as a means to treat neuropsychiatric disorders characterized by dysregulation in mPFC integration of long-range afferents with local inhibitory microcircuits.

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Relationship between regulation of morphine-induced EEG effects and changes in naloxone sensitivity

Paquette¹,

Young²

1991

European Journal of Pharmacology

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Modulation of morphine-induced EEG and behavioral effects by dynorphin A-(1-13) in non-tolerant and morphine-tolerant rats

Cited by 16 publications

References 20 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

Dynorphin / kappa-opioid receptor regulation of excitation-inhibition balance toggles afferent control of prefrontal cortical circuits in a pathway-specific manner

Relationship between regulation of morphine-induced EEG effects and changes in naloxone sensitivity

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