Hypocretin release in normal and narcoleptic dogs  after food and sleep deprivation, eating, and movement

Wu, Ming-Fung; John, Joshi; Maidment, Nigel T.; Lam, Hoa A.; Siegel, Jerome M.

doi:10.1152/ajpregu.00207.2002

Cited by 132 publications

(79 citation statements)

References 58 publications

(59 reference statements)

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“…Direct injection of orexin into the brain has been shown to increase alertness and muscle tone (Hagan et al, 1999;Bourgin et al, 2000;Piper et al, 2000). In addition several reports have demonstrated the correspondence between orexin-A release and the sleep-wake cycles of rodents, monkeys and humans (Edgar et Wu et al, 2002;Zeitzer et al, 2003;Lee et al, 2005). Orexin containing neurons are inactive in sleep and maximally active in waking states characterized by exploratory activity (Lee et al, 2005;Mileykovskiy et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Receptors for orexin-A are located on neurons in many different brain regions making it possible for this peptide, once released, to activate a large number of areas affected by sleep and sleep deprivation (Hagan et al, 1999;Bourgin et al, 2000;Kilduff and Peyron, 2000;Piper et al, 2000;Gerashchenko et al, 2001;Yoshida et al, 2001;Wu et al, 2002;Peever et al, 2003;Lee et al, 2005;Mileykovskiy et al, 2005;Vittoz and Berridge 2006), It has recently been shown that manipulation of this system via administration of a orexin antagonist can increase sleep in rats, dogs and humans (Brisbare-Roch et al, 2007). The loss of orexin cells has been shown to cause human and animal narcolepsy (Chemelli et al, 1999;Lin et al, 1999;Nishino et al, 2000;Peyron et al, 2000;Thannickal et al, 2000;Gerashchenko et al, 2001;Wu et al, 2002;Mieda et al, 2004). Orexin-A has been shown to produce arousal, increased attention, increased muscle tone and to counteract the effects of narcolepsy (Hagan et al, 1999;John et al, 2000;Siegel, 2004;Mileykovskiy et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Systemic and Nasal Delivery of Orexin-A (Hypocretin-1) Reduces the Effects of Sleep Deprivation on Cognitive Performance in Nonhuman Primates

Deadwyler¹,

Porrino²,

Siegel³

et al. 2007

J. Neurosci.

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242

192

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Hypocretin-1 (orexin-A) was administered to sleep-deprived (30 -36 h) rhesus monkeys immediately preceding testing on a multi-image delayed match-to-sample (DMS) short-term memory task. The DMS task used multiple delays and stimulus images and effectively measures cognitive defects produced by sleep deprivation (Porrino et al., 2005). Two methods of administration of orexin-A were tested, intravenous injections (2.5-10.0 g/kg, i.v.) and a novel method developed for nasal delivery via an atomizer spray mist to the nostrils (dose estimated 1.0 g/kg). Results showed that orexin-A delivered via the intravenous and nasal routes significantly improved performance in sleep-deprived monkeys; however, the nasal delivery method was significantly more effective than the highest dose (10 g/kg) of intravenous orexin-A tested. The improvement in performance by orexin-A was specific to trials classified as high versus low cognitive load as determined by performance difficulty under normal testing conditions. Except for the maximum intravenous dose (10 g/kg), neither delivery method affected task performance in alert non-sleep-deprived animals. The improved performance in sleep-deprived animals was accompanied by orexin-A related alterations in local cerebral glucose metabolism (CMRglc) in specific brain regions shown previously to be engaged by the task and impaired by sleep deprivation (Porrino et al., 2005). Consistent with the differential effects on performance, nasal delivered orexin-A produced a more pronounced reversal of sleep deprivation induced changes in brain metabolic activity (CMRglc) than intravenous orexin-A. These findings provide strong evidence for the effectiveness of intranasal orexin-A in alleviating cognitive deficits produced by loss of sleep.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Systemic and Nasal Delivery of Orexin-A (Hypocretin-1) Reduces the Effects of Sleep Deprivation on Cognitive Performance in Nonhuman Primates

Deadwyler¹,

Porrino²,

Siegel³

et al. 2007

J. Neurosci.

Self Cite

242

192

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“…Hypocretin has been shown to excite neurons in areas involved in the control of motoneuron activity such as the ventral tegmentum, locus coeruleus noradrenergic neurons, cholinergic and non-cholinergic neurons in the dorsolateral pontine tegmentum, and neurons in the nucleus pontis oralis (Hagan et al, 1999;Horvath et al, 1999;Ivanov and Aston-Jones, 2000;Nakamura et al, 2000;Burlet et al, 2002;Soffin et al, 2002;Xi et al, 2002). In addition, data recently provided by Kiyashchenco et al (2002) and Wu et al (2002) indicate that an increased release of Hcrt occurs during periods of wakefulness accompanied by movement. Furthermore, Torterolo et al (2003) found that Hcrt-containing neurons are activated only during behaviors that entail somatomotor activity [i.e., active wakefulness as well as carbachol-induced rapid eye movement (REM) sleep with its ancillary motor activity such as REMs and muscular twitches], whereas these neurons are not activated during wakefulness in the absence of movement or during quiet (non-REM) sleep.…”

Section: Considerations Of the Physiological Significance Of Hcrt Actmentioning

confidence: 99%

“…The hypocretinergic system has been suggested to play a role in a variety of physiological processes, most of which involve activation of the somatomotor system (Pu et al, 1998;Chemelli et al, 1999;Haynes et al, 1999;Lin et al, 1999;Siegel, 1999;Tamura et al, 1999;Kilduff and Peyron, 2000;Sutcliffe and de Lecea, 2000;Lin et al, 2002;Wu et al, 2002). Hcrtcontaining neurons project to regions that are involved in the generation of somatomotor activity Zhang et al, 2002) that provides a foundation for the concept that Hcrt is involved in the control of motor processes.…”

Section: Considerations Of the Physiological Significance Of Hcrt Actmentioning

confidence: 99%

Hypocretinergic Control of Spinal Cord Motoneurons

Yamuy

Fung²,

Xi³

et al. 2004

Journal of Neuroscience

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Hypocretinergic (orexinergic) neurons in the lateral hypothalamus project to motor columns in the lumbar spinal cord. Consequently, we sought to determine whether the hypocretinergic system modulates the electrical activity of motoneurons. Using in vivo intracellular recording techniques, we examined the response of spinal motoneurons in the cat to electrical stimulation of the lateral hypothalamus. In addition, we examined the membrane potential response to orthodromic stimulation and intracellular current injection before and after both hypothalamic stimulation and the juxtacellular application of hypocretin-1. It was found that (1) hypothalamic stimulation produced a complex sequence of depolarizing-hyperpolarizing potentials in spinal motoneurons; (2) the depolarizing potentials decreased in amplitude after the application of SB-334867, a hypocretin type 1 receptor antagonist; (3) the EPSP induced by dorsal root stimulation was not affected by the application of SB-334867; (4) subthreshold stimulation of dorsal roots and intracellular depolarizing current steps produced spike potentials when applied in concert to stimulation of the hypothalamus or after the local application of hypocretin-1; (5) the juxtacellular application of hypocretin-1 induced motoneuron depolarization and, frequently, high-frequency discharge; (6) hypocretin-1 produced a significant decrease in rheobase (36%), membrane time constant (16.4%), and the equalizing time constant (23.3%); (7) in a small number of motoneurons, hypocretin-1 produced an increase in the synaptic noise; and (8) the input resistance was not affected after hypocretin-1. The juxtacellular application of vehicle (saline) and denatured hypocretin-1 did not produce changes in the preceding electrophysiological properties.We conclude that hypothalamic hypocretinergic neurons are capable of modulating the activity of lumbar motoneurons through presynaptic and postsynaptic mechanisms. The lack of hypocretin-induced facilitation of motoneurons may be a critical component of the pathophysiology of cataplexy.

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“…This has been shown in several studies in order to evaluate the role of physical activity in OXA secretion of non-human subjects (9,13). In addition, some studies reported no change in OXA levels after physical activity in animal specimens (13,14).…”

Section: Introductionmentioning

confidence: 94%

Acute Aerobic Exercise and Plasma Levels of Orexin A, Insulin, Glucose, and Insulin Resistance in Males With Type 2 Diabetes

Alizadeh

Farhad

Hamid

et al. 2016

Jundishapur J Health Sci

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Background: The endocrine system disruptions are the main factors in metabolic disorders which are due to lifestyle changes, obesity, and aging. Insulin resistance is impaired glucose homeostasis in the presence of insulin and is related to many diseases such as hypertension, coronary artery disease, and type 2 diabetes Objectives: This study aimed to investigate the effect of acute aerobic exercise on plasma levels of orexin A, insulin, glucose, and insulin resistance in males with type 2 diabetes. Patients and Methods: Twenty subjects (mean age = 45.40 ± 5.42 years, mean weight = 80.91 ± 6.35 kg, body mass index = 25.41 ± 2.76 kg/ m 2 ) were randomly assigned into control and experimental groups, involving 10 people in each group. The exercise protocol consisted of one session of acute aerobic exercise on a treadmill at 60% maximal oxygen uptake and the same energy expenditure (300 kcal), which were determined by gas analyzers. Subjects were subjected to samplings before, immediately after, and 24 hours after the acute aerobic exercise. Results:The analysis of findings in P ≤ 0.05 indicated that acute aerobic exercise caused a significant increase in plasma levels of orexin A and a significant decrease in plasma levels of glucose immediately after the aerobic activity, but insignificantly affected the plasma levels of insulin and insulin resistance. Conclusions: It seems that in people with type 2 diabetes, acute aerobic exercise can decrease the plasma levels of glucose, possibly through increasing orexin A. In addition, negative energy balance is necessary to decrease the levels of insulin and insulin resistance during acute aerobic exercise.

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Hypocretin release in normal and narcoleptic dogs after food and sleep deprivation, eating, and movement

Abstract: release in normal and narcoleptic dogs after food and sleep deprivation, eating, and movement. Am

Cited by 132 publications

References 58 publications

Systemic and Nasal Delivery of Orexin-A (Hypocretin-1) Reduces the Effects of Sleep Deprivation on Cognitive Performance in Nonhuman Primates

Systemic and Nasal Delivery of Orexin-A (Hypocretin-1) Reduces the Effects of Sleep Deprivation on Cognitive Performance in Nonhuman Primates

Hypocretinergic Control of Spinal Cord Motoneurons

Acute Aerobic Exercise and Plasma Levels of Orexin A, Insulin, Glucose, and Insulin Resistance in Males With Type 2 Diabetes

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