Opioids, Sedation, and Sleep: Different States, Similar Traits, and the Search for Common Mechanisms

Lydic, Ralph; Baghdoyan, Helen A.; McGinley, Jacinta

doi:10.1385/1-59259-295-3:1

Cited by 4 publications

(6 citation statements)

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“…Sleep is the behavioral state most thoroughly characterized at the cellular level. 4,26 The extensive range of drugs used to create states of anesthesia 45 and sedation 51 adds to the complexity of defining these states based on a constellation of neurobiological traits. Clinical practice guidelines from the American Society of Anesthesiologists (ASA) describe states of sedation as a continuum ranging from minimal sedation involving anxiolysis, to conscious sedation during which patients can respond to verbal input, to states of deep sedation in which patients respond only to painful stimulation.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine-Induced Sedation Does Not Mimic the Neurobehavioral Phenotypes of Sleep in Sprague Dawley Rat

Garrity

Botta

Lazar

et al. 2015

Sleep

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Section: Discussionmentioning

confidence: 99%

Dexmedetomidine-Induced Sedation Does Not Mimic the Neurobehavioral Phenotypes of Sleep in Sprague Dawley Rat

Garrity

Botta

Lazar

et al. 2015

Sleep

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“…Drugs used in insomnia treatment (melatonin and melatonin analogues) exert their effects via MT1 and MT2 receptors. Other hypnotic substances acting through GABA (Valerian preparations, Gabapentin, Tiagabine), Sedative antipsychotics (Olanzapine, quetiapine; they are 5HT-2A antagonists), Gamma hydroxybutyrate (its mechanism of effect is not fully understood, it is considered to modulate dopamine activity; it is recommended in narcolepsy for cataplexy treatment) [14,15,55,56].…”

Section: Anesthetics Sedatives and Hypnoticsmentioning

confidence: 99%

Neurophysiology of Basic Molecules Affecting Sleep and Wakefulness Mechanisms, Fundamentals of Sleep Pharmacology

Kayabekir¹

2022

Sleep Medicine and the Evolution of Contemporary Sleep Pharmacotherapy

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As part of the biological rhythm, the human brain has a healthy functioning with the ability to differentiate between day and night hours in any given day (sleep rhythm, life rhythm). From the control of hormone levels to muscle tonus, from the regulation of respiratory rate to the content of our thoughts, sleep has an impact on all bodily and cognitive functions. It is not surprising to see such effects of sleep on the body as it leads to significant changes in the electrical activity of the brain in general. Electrical signal changes in the brain (sleep-wakefulness rhythm) are regulated by neurohormonal molecules and their receptors in the body. Neurotransmitters that control sleep and wakefulness can be listed as “Glutamate, Acetylcholine, Histamine, Norepinephrine and GABA”. Main hormones are: Melatonin, Corticotropin Releasing Hormone (CRH), cortisol, prolactin, Growth Hormone (GH), Insulin like Growth Factor (IGF-1, Somatomedin-C), Follicle Stimulating Hormone (FSH) and Luteinizing Hormone (LH), progesterone, estrogen, testosterone, catecholamines, leptin and neuropeptide Y″. The effects of pharmacological agents on sleep and wakefulness cycles are materialized through the following molecules and their receptors: Hypnotics (GABA A agonists, benzodiazepines, gabapentin, tiagabine), sedative antidepressants (tricyclic antidepressants, trazadone, mitrazapine), antihistamines, medications used for the treatment of sleeplessness (melatonin and melatonin analogues), amphetamine (most commonly used stimulant), secretion of monoamines (dopamine), non-amphetamine stimulants used in the treatment of hypersomnia and narcolepsy (modafinil, bupropion, selegiline, caffeine) and other substances (alcohol, nicotine, anesthetics). To the extent we can conceptualize the physiological mechanisms of these basic molecules listed above and the regions they affect, we can appreciate the effects of these substances on sleep physiology and sleep disorders.

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“…282 Central chemosensitivity now is known to involve many brain regions in addition to the ventrolateral surface of the medulla. 289 The tongue muscle is believed to block the upper airway in many cases of OSA. 9D).…”

Section: Traits Defining States: Nociceptionmentioning

confidence: 99%

“…280 The implication of these findings is that endogenous acetylcholine in the pontine reticular formation contributes to the respiratory changes characteristic of sleep. 304,305 As reviewed elsewhere, 289 serotonin can facilitate respiratory drive to upper airway muscles, and activation of ␣ 2 adrenoreceptors can depress respiratory neurons and the ability to respond to hypercapnia. 285 Opioids continue to serve as the analgesic drug of choice despite the potential side effect of respiratory depression and being a leading cause of postoperative nausea and vomiting.…”

Section: Traits Defining States: Nociceptionmentioning

confidence: 99%

“…333 Sleep deprivation is deleterious to both anesthesiologist and patient because memory and arousal functions subserved by prefrontal cortex are especially vulnerable to sleep deprivation 137,334 -336 and anesthesia. 289 Prolonged wakefulness increases rat brain levels of adenosine, 351 and caffeine ingestion by humans increases latency to sleep onset and reduces the electroencephalographic delta power of NREM sleep. [265][266][267][268] Adenosine Dephosphorylation of adenosine triphosphate produces adenosine, and all cellular activities that increase metabolic demand will increase adenosine.…”

Section: Arousal States Are Regulated By Multiple Neurotransmitters Amentioning

confidence: 99%

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Sleep, Anesthesiology, and the Neurobiology of Arousal State Control

Lydic

Baghdoyan

2005

Anesthesiology

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Sleep, like breathing, is a biologic rhythm that is actively generated by the brain. Neuronal networks that have evolved to regulate naturally occurring sleep preferentially modulate traits that define states of sedation and anesthesia. Sleep is temporally organized into distinct stages that are characterized by a unique constellation of physiologic and behavioral traits. Sleep and anesthetic susceptibility are genetically modulated, heritable phenotypes. This review considers 40 yr of research regarding the cellular and molecular mechanisms contributing to arousal state control. Clinical and preclinical data have debunked and supplanted the primitive view that sleep need is a weakness. Sleep deprivation and restriction diminish vigilance, alter neuroendocrine control, and negatively impact immune function. There is overwhelming support for the view that decrements in vigilance can negatively impact performance. Advances in neuroscience provide a foundation for the sea change in public and legal perspectives that now regard a sleepdeprived individual as impaired.

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Opioids, Sedation, and Sleep: Different States, Similar Traits, and the Search for Common Mechanisms

Cited by 4 publications

References 0 publications

Dexmedetomidine-Induced Sedation Does Not Mimic the Neurobehavioral Phenotypes of Sleep in Sprague Dawley Rat

Dexmedetomidine-Induced Sedation Does Not Mimic the Neurobehavioral Phenotypes of Sleep in Sprague Dawley Rat

Neurophysiology of Basic Molecules Affecting Sleep and Wakefulness Mechanisms, Fundamentals of Sleep Pharmacology

Sleep, Anesthesiology, and the Neurobiology of Arousal State Control

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