Hypocretinergic neurons are activated in conjunction with goal-oriented survival-related motor behaviors

Torterolo, Pablo; Ramos, Oscar V.; Sampogna, Sharon; Chase, Michael H.

doi:10.1016/j.physbeh.2011.07.032

Cited by 22 publications

(16 citation statements)

References 65 publications

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“…Hypocretinergic neurons project directly to motoneurons, and produce motor activation during emotionallydriven or survival-related waking behaviors [41][42][43][44][45]. Following a emotional stimuli, due to the dysfunction of the hypocretinergic system there is a drastic reduction in the degree of activation of the somatic motor system and/or, the REM sleep atonia network may be inadequately activated [46], which may be responsible for the episodes of cataplexy [13].…”

Section: Hrv During Cataplexy Induced By Carbacholmentioning

confidence: 99%

Heart rate variability during carbachol-induced REM sleep and cataplexy

Torterolo

Castro-Zaballa

Cavelli

et al. 2015

Behavioural Brain Research

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Section: Hrv During Cataplexy Induced By Carbacholmentioning

confidence: 99%

Heart rate variability during carbachol-induced REM sleep and cataplexy

Torterolo

Castro-Zaballa

Cavelli

et al. 2015

Behavioural Brain Research

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“…Presumably, this regular diurnal removal of TNF would allow the activity of orexigenic neurons in the lateral hypothalamus to rise each morning, gearing up the individual to face the challenges of the day [51]. The more profound question is why, as each awake period progresses, the rise in TNF [33] and Aβ [49] in CSF should occur.…”

Section: Implications For Normal Diurnal Changes In Brain Inflammatormentioning

confidence: 99%

Inflammation-sleep interface in brain disease: TNF, insulin, orexin

Clark

Vissel

2014

J Neuroinflammation

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The depth, pattern, timing and duration of unconsciousness, including sleep, vary greatly in inflammatory disease, and are regarded as reliable indicators of disease severity. Similarly, these indicators are applicable to the encephalopathies of sepsis, malaria, and trypanosomiasis, and to viral diseases such as influenza and AIDS. They are also applicable to sterile neuroinflammatory states, including Alzheimer’s disease, Parkinson’s disease, traumatic brain injury, stroke and type-2 diabetes, as well as in iatrogenic brain states following brain irradiation and chemotherapy. Here we make the case that the cycles of unconsciousness that constitute normal sleep, as well as its aberrations, which range from sickness behavior through daytime sleepiness to the coma of inflammatory disease states, have common origins that involve increased inflammatory cytokines and consequent insulin resistance and loss of appetite due to reduction in orexigenic activity. Orexin reduction has broad implications, which are as yet little appreciated in the chronic inflammatory conditions listed, whether they be infectious or sterile in origin. Not only is reduction in orexin levels characterized by loss of appetite, it is associated with inappropriate and excessive sleep and, when dramatic and chronic, leads to coma. Moreover, such reduction is associated with impaired cognition and a reduction in motor control. We propose that advanced understanding and appreciation of the importance of orexin as a key regulator of pathways involved in the maintenance of normal appetite, sleep patterns, cognition, and motor control may afford novel treatment opportunities.

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“…The administration of hypocretin promotes arousal; when there is a deficiency in hypocretin, there is a corresponding decrease in wakefulness and the ability of animals to respond to alerting stimuli (118,132). Importantly, it has been shown that hypocretinergic neurons are selectively activated during arousal that is associated with the enactment of survival behaviors; however, arousal that occurs in the absence of such behaviors is not correlated with an increase in the discharge of hypocretinergic neurons (160,163).…”

Section: Hypocretinergic Actions In Response To Survival Stimulimentioning

confidence: 99%

A unified survival theory of the functioning of the hypocretinergic system

Chase

2013

Journal of Applied Physiology

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This article advances the theory that the hypocretinergic (orexinergic) system initiates, coordinates, and maintains survival behaviors and survival-related processes (i.e., the Unified Survival Theory of the Functioning of the Hypocretinergic System or "Unified Hypocretinergic Survival Theory"). A priori presumptive support for the Unified Hypocretinergic Survival Theory emanates from the fact that neurons that contain hypocretin are located in the key executive central nervous system (CNS) site, the lateral hypothalamus, that for decades has been well-documented to govern core survival behaviors such as fight, flight, and food consumption. In addition, the hypocretinergic system exhibits the requisite morphological and electrophysiological capabilities to control survival behaviors and related processes. Complementary behavioral data demonstrate that all facets of "survival" are coordinated by the hypocretinergic system and that hypocretinergic directives are not promulgated except during survival behaviors. Importantly, it has been shown that survival behaviors are selectively impacted when the hypocretinergic system is impaired or rendered nonfunctional, whereas other behaviors are relatively unaffected. The Unified Hypocretinergic Survival Theory resolves the disparate, perplexing, and often paradoxical-appearing results of previous studies; it also provides a foundation for future hypothesis-driven basic science and clinical explorations of the hypocretinergic system.

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Hypocretinergic neurons are activated in conjunction with goal-oriented survival-related motor behaviors

Cited by 22 publications

References 65 publications

Heart rate variability during carbachol-induced REM sleep and cataplexy

Heart rate variability during carbachol-induced REM sleep and cataplexy

Inflammation-sleep interface in brain disease: TNF, insulin, orexin

A unified survival theory of the functioning of the hypocretinergic system

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