![]() Wild-type female mice were placed into the home cage of male ORX-AB and cataplexy-like behavior was observed along with ultrasonic vocalizations (USVs), also known as the "love song". To further evaluate mice's cataplexy, we examined courtship behavior in orexin neuron-ablated mice (ORX-AB), one of the animal models of narcolepsy/cataplexy. , Procedimientos Quirúrgicos Operativos/efectos adversosĬataplexy is triggered by laughter in humans and palatable food in mice. , Trastornos del Inicio y del Mantenimiento del Sueño/fisiopatología , Trastornos del Inicio y del Mantenimiento del Sueño/diagnóstico , Trastornos del Inicio y del Mantenimiento del Sueño/complicaciones , Síndrome de las Piernas Inquietas/fisiopatología , Síndrome de las Piernas Inquietas/diagnóstico , Síndrome de las Piernas Inquietas/complicaciones ![]() , Complicaciones Posoperatorias/fisiopatología , Complicaciones Posoperatorias/etiología , Atención Perioperativa/efectos adversos , Trastornos del Inicio y del Mantenimiento del Sueño/terapia , Síndrome de las Piernas Inquietas/terapia This review will highlight the current state of the literature and offer recommendations for management of these conditions during the perioperative journey. There are a number of mechanisms by which such common sleep disorders (eg, insomnia, restless legs syndrome, narcolepsy, and parasomnias) may have consequences in the perioperative setting, both related to the underlying pathophysiology of the diseases as well as their treatments. More recently, investigators have begun to examine other common sleep disorders to assess how they may be impacted by the perioperative environment, as well as influence postoperative outcomes. Obstructive sleep apnea (OSA) has been shown to increase risk of adverse perioperative events. The availability of novel devices measuring sleep 24 h per day also holds promise to provide new insights into how brain electrical activity and muscle tone are regulated by hypocretin. Novel technologies, such as the use of deep learning analysis of electroencephalographic signals, is revealing a complex pattern of sleep abnormalities in human narcolepsy that can be used diagnostically. Narcolepsy is also associated with an inability to consolidate sleep, a more complex phenotype that may result from secondary changes or be central to the role of hypocretin in coordinating the activity of other sleep- and wake-promoting systems. Current analyses suggest that the main functions of the hypocretin/orexin system are (1) maintenance of wakefulness in the face of moderate sleep deprivation (2) passive wake promotion, especially in the evening, driven by the circadian clock (3) inhibition of REM sleep, with possible differential modulating effects on various subcomponents of the sleep-stage, explaining REM sleep dissociation events in NT1. The discovery that NT1 is caused by hypocretin/orexin deficiency, together with neurochemical studies of this system, has helped to establish how this neuropeptide regulates the organization of sleep and wake in humans. Since its description in the 19th century, narcolepsy type 1 (NT1) has been considered as a model sleep disorder, and after the discovery of rapid eye movement (REM) sleep onset in the disorder, a gateway to understanding REM sleep. , Proteínas del Tejido Nervioso/metabolismo , Área Hipotalámica Lateral/fisiopatología Our findings demonstrate a mechanism underlying sleep instability during aging and a strategy to improve sleep continuity. Disruption of Kcnq2/3 genes in Hcrt neurons of young mice destabilized sleep, mimicking aging-associated sleep fragmentation, whereas the KCNQ-selective activator flupirtine hyperpolarized Hcrt neurons and rejuvenated sleep architecture in aged mice. Single-nucleus RNA-sequencing revealed adaptive changes to Hcrt neuron loss in the aging brain. Aged Hcrt neurons showed hyperexcitability with lower KCNQ2 expression and impaired M-current, mediated by KCNQ2/3 channels. In aged mice, Hcrt neurons exhibited more frequent neuronal activity epochs driving wake bouts, and optogenetic activation of Hcrt neurons elicited more prolonged wakefulness. ![]() We found that hyperexcitable hypocretin/orexin (Hcrt/OX) neurons drive sleep fragmentation during aging. Sleep quality declines with age however, the underlying mechanisms remain elusive.
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