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Orexin-A 5mg

Item 12760

Sleep, Eat, Sex – Orexin Has Something to Say

Orexin is a neuropeptide which is released by the posterior lateral hypothalamus, and is linked to wakefulness and sleep, appetite regulation, and the motivation of sexual and addictive behaviors.  One apt way to think about it is as a hormone in the brain, combining some of the popularly conceived effects of adrenaline and testosterone into one. 

(Don’t get too excited now!  I am just trying to give you a way to think about it, that orexin works to promote arousal and response…)

I am writing a post on the links of orexin to appetitive behavior, particularly addiction, but I’ve generated a lot of material.  So I am going to give you this one first, which summarizes aspects of orexin (also known as hypocretin) and neurological function with respect to sleep, appetite and sex. 


Orexin is definitely involved in arousal and wakefulness, for example, in getting sleepy or drowsy people to be more awake (with little effect on arousal in already rested individuals).  In other words, orexin might be a way to combat fatigue in the future.  There’s a whole Wired article, Snorting a Brain Chemical Could Replace Sleep, on it.  As the Wired article puts it, “it cures sleepiness,” at least in monkeys in some pretty controlled conditions.  Besides treatment of narcolepsy, other possible uses being considered are for pilots on long flights and people suffering from jet lag.

 For the science behind it, there are some links: Promoting Wakefulness: http://www.jneurosci.org/cgi/content/abstract/27/52/14239; Possible Sleep Medication: http://www.nature.com/nm/journal/v13/n2/abs/nm1544.html; Narcolepsy & Low Orexin: http://www.pnas.org/cgi/reprint/0400590101v1.pdf 


Orexin plays a key role in promoting eating and appetite, and seems to work to signal “eat more.”  It’s hypothesized as one main component for getting people to eat beyond satiety (and here I thought Thanksgiving dinners were the reason).  

 For example, Rodgers et al. (2002) argue, “These data suggest that orexin-1 receptors mediate the episodic signalling of satiety and appear to bridge the transition from eating to resting in the rats’ feeding-sleep cycle. The argument is developed that the diverse physiological and behavioural effects of orexins can best be understood in terms of an integrated set of reactions which function to rectify nutritional status without compromising personal survival.”

 Or, in this report “Obesity: Is It In Your Head?,” the reporter notes, “Some brains may be wired to encourage fidgeting and other restless behaviors that consume calories and help control weight, according to new research published by The American Physiological Society.  The study found that the brains of rats bred to be lean are more sensitive to a chemical produced in the brain, orexin A, which stimulates appetite and spontaneous physical activity such as fidgeting and other unconscious movements. Compared to rats bred to be obese, the lean rats had a far greater expression of orexin receptors in the hypothalamus.  ‘The greater expression of orexin receptors suggests the lean rats’ brains were more sensitive to the orexin the brain produces,’ said Catherine M. Kotz, the study’s senior researcher.”

 Other research shows orexin plays a role in increased sensitivity to sensory cues.  Julliard et al. (2007) write, “Orexin therefore increases and leptin decreases olfactory sensitivity. Orexin and leptin modulate the olfactory performance in a similar way as do physiological induced fasting and satiation and appear to be important factors in the interdependency of olfaction and food intake.”  In other words, orexin on its own makes rats as sensitive to olfactory cues as being hungry. 

To sum up, orexin plays a role in driving eating beyond satiety and in sedentary behavioral inclinations, as well as in sensory sensitivity.  In turn, these connect to exercise, environmental cues, emotions, and cognition.  Put differently, our culture can drive our biology, particularly in the domain of appetite, into realms of excess.  That is the basic conclusion, in my mind, of the following article “Eating for Pleasure or Calories.”  The abstract reads:

A changing environment and lifestyle on the background of evolutionary engraved or perinatally imprinted physiological response patterns is the foremost explanation for the current obesity epidemic. However, it is not clear what the mechanisms are by which the modern environment overrides the physiological controls of appetite and homeostatic body weight regulation. Major advances have been made regarding crosstalk between metabolic signals and the cognitive/emotional brain that primarily deals with the environment. On one hand, metabolic signals such as leptin and ghrelin have previously unexpected direct effects on learning and memory, as well as liking and wanting. On the other hand, brain areas involved in reward, cognition, and executive control can override metabolic regulation by talking to the hypothalamus. 


As one article puts it, “Besides playing a role in the regulation of feeding and energy homeostasis in rats, ORs appear to increase sexual arousal as well as copulatory performance in rats.”

 So here’s one relevant piece by Guliaa et al. (2003): “The medial preoptic area plays an important role in the regulation of male sexual behavior in rats, and this area receives orexinergic inputs… The results of the study showed that orexin A application at the medial preoptic area increased sexual arousal as well as the copulatory performance. Sexual arousal is one of the physiological stimuli, which influences wakefulness.”  (I can see the pharmaceutical companies now—rather a cigarette, have a little nasal orexin and another go-round.)

And a more recent article by Muschamp et al. (2007), which concludes “Together, these data support the view that hcrt/orx peptides may act in a steroid-sensitive manner to facilitate the energized pursuit of natural rewards like sex via activation of the mesolimbic DA system.”



Orexins, also called hypocretins, are the common names given to a pair of excitatory neuropeptide hormones that were simultaneously discovered by two groups of researchers in rat brains.[1][2]

The two related peptides (Orexin-A and B, or hypocretin-1 and -2), with approximately 50% sequence identity, are produced by cleavage of a single precursor protein. Orexin-A/hypocretin-1 is 33 amino acid residues long and has two intrachain disulfide bonds, while Orexin-B/hypocretin-2 is a linear 28 amino acid residue peptide. Studies suggest that orexin A/hypocretin-1 may be of greater biological importance than orexin B/hypocretin-2. Although these peptides are produced by a very small population of cells in the lateral and posterior hypothalamus, they send projections throughout the brain. The orexin peptides bind to the two G-protein coupled orexin receptors, OX1 and OX2, with Orexin-A binding to both OX1 and OX2 with approximately equal affinity while Orexin-B binds mainly to OX2 and is 5 times less potent at OX1.[3]

The orexins/hypocretins are strongly conserved peptides, found in all major classes of vertebrates


The orexin/hypocretin system was initially suggested to be primarily involved in the stimulation of food intake, based on the finding that central administration of orexin A/hypocretin-1 increases food intake. In addition, it stimulates wakefulness and energy expenditure.


Orexin seems to promote wakefulness. Recent studies indicate that a major role of the orexin/hypocretin system is to integrate metabolic, circadian and sleep debt influences to determine whether an animal should be asleep or awake and active. Orexin/hypocretin neurons strongly excite various brain nuclei with important roles in wakefulness including the dopamine, norepinephrine, histamine and acetylcholine systems[4][5] and appear to play an important role in stabilizing wakefulness and sleep.

The discovery that an orexin/hypocretin receptor mutation causes the sleep disorder canine narcolepsy[6] in Doberman Pinschers subsequently indicated a major role for this system in sleep regulation. Genetic knockout mice lacking the gene for orexin were also reported to exhibit narcolepsy.[7] Transitioning frequently and rapidly between sleep and wakefulness, these mice display many of the symptoms of narcolepsy. Researchers are using this animal model of narcolepsy to study the disease.[8] Narcolepsy results in excessive daytime sleepiness, inability to consolidate wakefulness in the day (and sleep at night), and cataplexy, which is the loss of muscle tone in response to strong, usually positive, emotions. Dogs that lack a functional receptor for orexin/hypocretin have narcolepsy, while animals and people lacking the orexin/hypocretin neuropeptide itself also have narcolepsy.

Central administration of orexin A/hypocretin-1 strongly promotes wakefulness, increases body temperature, locomotion and elicits a strong increase in energy expenditure. Sleep deprivation also increases orexin A/hypocretin-1 transmission. The orexin/hypocretin system may thus be more important in the regulation of energy expenditure than food intake. In fact, orexin/hypocretin-deficient narcoleptic patients have increased obesity rather than decreased BMI, as would be expected if orexin/hypocretin were primarily an appetite stimulating peptide. Another indication that deficits of orexin/hypocretin cause narcolepsy is that depriving monkeys of sleep for 30–36 hours and then injecting them with the neurochemical alleviates the cognitive deficiencies normally seen with such amount of sleep loss.[9][10]

In humans, narcolepsy is associated with a specific variant of the human leukocyte antigen (HLA) complex.[11] Furthermore, genome-wide analysis shows that, in addition to the HLA variant, narcoleptic humans also exhibit a specific genetic mutation in the T-cell receptor alpha locus.[12] In conjunction, these genetic anomalies cause the autoimmune system to attack and kill the critical hypocretin neurons. Hence the absence of hypocretin-producing neurons in narcoleptic humans may be the result of an autoimmune disorder.[13]

Wakefulness, amyloid beta, and Alzheimer's disease

A link between orexin and Alzheimer's disease has been recently suggested.[14] The enigmatic protein amyloid beta builds up over time in the brain and is correlated with Alzheimer's disease. The recent research shows that amyloid beta expression rises during the day and falls during the night, and that this is controlled by orexin.[14] Sleep deprivation is suggested to lead to amyloid beta plaque development.[14] It is suggested that drugs that block orexin receptors could be used to modulate amyloid beta build-up.[14] This research also suggests that maintaining proper lengths of sleep and wake periods could prevent Alzheimer's disease, assuming that 1) amyloid beta is the cause of Alzheimer's disease and 2) that sleep-wake cycling rather than some other cause is what leads to the amyloid beta build-up in the brains of people with Alzheimer's disease — two claims that have not been demonstrated.

Food intake

Orexin increases the craving for food, and correlates with the function of the substances that promote its production.

Leptin is a hormone produced by fat cells and acts as a long-term internal measure of energy state. Ghrelin is a short-term factor secreted by the stomach just before an expected meal, and strongly promotes food intake.

Hypocretin-producing cells have recently been shown to be inhibited by leptin (through the leptin receptor pathway), but are activated by ghrelin and hypoglycemia (glucose inhibits orexin production). Orexin/hypocretin, as of 2007, is claimed to be a very important link between metabolism and sleep regulation.[citation needed] Such a relationship has been long suspected, based on the observation that long-term sleep deprivation in rodents dramatically increases food intake and energy metabolism, i.e., catabolism, with lethal consequences on a long-term basis.

Pharmacologic potential

The research on orexin/hypocretin is still in an early phase, although many scientists believe that orexin/hypocretin-based drugs could help narcoleptics and increase alertness in the brain without the side effects of amphetamines.

Preliminary research has been conducted that shows potential for orexin blockers in the treatment of alcoholism. Lab rats given drugs which targeted the orexin system lost interest in alcohol despite being given free access in experiments.[15][16]

A study has reported that transplantation of orexin/hypocretin neurons into the pontine reticular formation in rats is feasible, indicating the development of alternative therapeutic strategies in addition to pharmacological interventions to treat narcolepsy.[17]

Because hypocretin-1 receptors have been shown to regulate relapse to cocaine seeking, a new study investigated its relation to nicotine by studying rats. By blocking the hypocretin-1 receptor with low doses of the selective antagonist SB-334,867, nicotine self-administration decreased and also the motivation to seek and obtain the drug. The study showed that blocking of receptors in the insula decreased self-administration, but not blocking of receptors in the adjacent somatosensory cortex. The greatest decrease in self-administration was found when blocking all hypocretin-1 receptors in the brain as a whole. A rationale for this study was the fact that the insula has been implicated in regulating feelings of craving. The insula contains hypocretin-1 receptors. It has been reported that smokers who sustained damage to the insula lost the desire to smoke.[18]

Lipid metabolism

Orexin-A (OXA) has been recently demonstrated to have direct effect on a part of the lipid metabolism. OXA stimulates glucose uptake in 3T3-L1 adipocytes and that increased energy uptake is stored as lipids (triacylglycerol). OXA thus increases lipogenesis. It also inhibits lipolysis and stimulates the secretion of adiponectin. These effects are thought to be mostly conferred via the PI3K pathway because this pathway inhibitor (LY294002) completely blocks OXA effects in adipocytes[19]. The link between OXA and the lipid metabolism is new and currently under more research.

Obesity in orexin-knockout mice is associated with impaired brown adipose tissue thermogenesis.[20]

History and nomenclature

In 1996, Gautvik, de Lecea, and colleagues reported the discovery of several genes in the rat brain, including one they dubbed "clone 35." Their work showed that clone 35 expression was limited to the lateral hypothalamus.[21] Two years later they would identify the two genetic products of clone 35 as the hypocretins.

Masashi Yanagisawa and colleagues at the University of Texas Southwestern Medical Center at Dallas, coined the term orexin to reflect the orexigenic (appetite-stimulating) activity of these hormones. In their 1998 paper (with authorship attributed to Sakurai and colleagues) describing these neuropeptides, they also reported discovery of two orexin receptors, dubbed OX1R and OX2R.[1]

Luis de Lecea, Thomas Kilduff, and colleagues also reported discovery of these same peptides, dubbing them hypocretins to indicate that they are synthesized in the hypothalamus and to reflect their structural similarity to the hormone secretin (i.e., hypothalamic secretin). This is the same group that first identified clone 35 two years earlier.[2][21]

The name of this family of peptides is currently an unsettled issue. The name "orexin" has been rejected by some due to evidence that the orexigenic effects of these peptides may be incidental or trivial (i.e., hypocretin induced subjects eat more because they are awake more), though this issue is also unsettled, while other groups maintain that the name "hypocretin" is awkward, pointing out that many neuropeptides have names that are unrelated to their most important functions, and that waking is one of the important factors that supports feeding behavior. Both "orexin" and "hypocretin" will likely continue to appear in published works until a preferred name has been accepted by the scientific community.

Selective ligands

Several drugs acting on the orexin system are under development, either orexin agonists for the treatment of conditions such as narcolepsy, or orexin antagonists for insomnia. No non-peptide agonists are yet available, although synthetic Orexin-A polypeptide has been made available as a nasal spray and tested on monkeys. Several non-peptide antagonists are in development however; SB-649,868 is under development by GlaxoSmithKline for sleep disorders and is a non-selective orexin receptor antagonist. Another OX1 and OX2 receptor antagonist (ACT-078573, almorexant) is a similar compound under development for primary insomnia by Actelion. A third entry is Merck's MK-4305.[22]

Most ligands acting on the orexin system so far are polypeptides modified from the endogenous agonists Orexin-A and Orexin-B, however there are some subtype-selective non-peptide antagonists available for research purposes.

Interaction with other neurotransmitter systems

Orexinergic neurons have been shown to be sensitive to inputs from Group III metabotropic glutamate receptors,[23] adenosine A1 receptors,[24] muscarinic M3 receptors,[25] serotonin 5-HT1A receptors,[26] neuropeptide Y receptors,[27] cholecystokinin A receptors,[28] and catecholamines,[29][30] as well as to ghrelin, leptin, and glucose.[31] Orexinergic neurons themselves regulate release of acetylcholine,[32][33] serotonin and noradrenaline,[34] so despite the relatively small number of orexinergic neurons compared to other neurotransmitter systems in the brain, this system plays a key regulatory role and extensive research will be required to unravel the details. Orexins act on Gq-protein-coupled receptors signaling through phospholipase C (PLC) and calcium-dependent as well as calcium-independent transduction pathways. These include activation of electrogenic sodium-calcium exchangers (NCX) and a non-specific cationic conductance, likely channels of the transient receptor potential canonical-(TRPC) type activation of L-type voltage-dependent calcium channels, closure of G-protein-activated inward rectifier potassium channels (GIRK), and activation of protein kinases, including protein kinase C (PKC), protein kinase A (PKA), and mitogen-associated protein kinase, also called mitogen-activated protein kinase (MAPK). Postsynaptic actions of orexins on their numerous neuronal targets throughout the CNS are almost entirely excitatory.[35]


1.      ^ a b Sakurai T, Amemiya A, Ishii M, Matsuzaki I, Chemelli RM, Tanaka H, Williams SC, Richardson JA, Kozlowski GP, Wilson S, Arch JR, Buckingham RE, Haynes AC, Carr SA, Annan RS, McNulty DE, Liu WS, Terrett JA, Elshourbagy NA, Bergsma DJ, Yanagisawa M (1998). "Orexins and orexin receptors: a family of hypothalamic neuropeptides and G protein-coupled receptors that regulate feeding behavior". Cell 92 (4): 573–85. doi:10.1016/S0092-8674(00)80949-6. PMID 9491897.

2.      ^ a b de Lecea L, Kilduff TS, Peyron C, Gao X, Foye PE, Danielson PE, Fukuhara C, Battenberg EL, Gautvik VT, Bartlett FS, Frankel WN, van den Pol AN, Bloom FE, Gautvik KM, Sutcliffe JG (1998). "The hypocretins: hypothalamus-specific peptides with neuroexcitatory activity". Proc. Natl. Acad. Sci. U.S.A. 95 (1): 322–7. doi:10.1073/pnas.95.1.322. PMC 18213. PMID 9419374.

3.      ^ Langmead CJ, Jerman JC, Brough SJ, Scott C, Porter RA, Herdon HJ (January 2004). "Characterisation of the binding of [3H-SB-674042, a novel nonpeptide antagonist, to the human orexin-1 receptor"]. Br. J. Pharmacol. 141 (2): 340–6. doi:10.1038/sj.bjp.0705610. PMC 1574197. PMID 14691055.

4.      ^ Sherin JE, Elmquist JK, Torrealba F, Saper CB (June 1998). "Innervation of histaminergic tuberomammillary neurons by GABAergic and galaninergic neurons in the ventrolateral preoptic nucleus of the rat". J. Neurosci. 18 (12): 4705–21. PMID 9614245.

5.      ^ Lu J, Bjorkum AA, Xu M, Gaus SE, Shiromani PJ, Saper CB (June 2002). "Selective activation of the extended ventrolateral preoptic nucleus during rapid eye movement sleep". J. Neurosci. 22 (11): 4568–76. PMID 12040064.

6.      ^ Lin L, Faraco J, et. al. (1999). "The sleep disorder canine narcolepsy is caused by a mutation in the hypocretin (orexin) receptor 2 gene.". Cell 98 (3): 365–376. doi:10.1016/S0092-8674(00)81965-0. PMID 10458611.

7.      ^ Chemelli RM, Willie JT, et. al. (1999). "Narcolepsy in orexin knockout mice: molecular genetics of sleep regulation.". Cell 98 (4): 437–451. doi:10.1016/S0092-8674(00)81973-X. PMID 10481909.

8.      ^ Mochizuki T, Crocker A, McCormack S, Yanagisawa M, Sakurai T, Scammell TE (July 2004). "Behavioral state instability in orexin knock-out mice". J. Neurosci. 24 (28): 6291–300. doi:10.1523/JNEUROSCI.0586-04.2004. PMID 15254084.

9.      ^ Alexis Madrigal (2007-12-28). "Snorting a Brain Chemical Could Replace Sleep". Wired News, Condé Nast. Retrieved 2008-02-05.

10.  ^ Deadwyler SA, Porrino L, Siegel JM, Hampson RE (2007). "Systemic and nasal delivery of orexin-A (Hypocretin-1) reduces the effects of sleep deprivation on cognitive performance in nonhuman primates". J. Neurosci. 27 (52): 14239–47. doi:10.1523/JNEUROSCI.3878-07.2007. PMID 18160631.

11.  ^ Klein J, Sato A (September 2000). "The HLA system. Second of two parts". N. Engl. J. Med. 343 (11): 782–6. doi:10.1056/NEJM200009143431106. PMID 10984567.

12.  ^ Hallmayer J, Faraco J, Lin L, et al. (June 2009). "Narcolepsy is strongly associated with the T-cell receptor alpha locus". Nat. Genet. 41 (6): 708–11. doi:10.1038/ng.372. PMC 2803042. PMID 19412176.

13.  ^ "Narcolepsy is an autoimmune disorder, Stanford researcher says". EurekAlert. American Association for the Advancement of Science. 2009-05-03. Retrieved 2009-05-31.

14.  ^ a b c d J. E. Kang, M. M. Lim, R. J. Bateman, J. J. Lee, L. P. Smyth, J. R. Cirrito, N. Fujiki, S. Nishino and D. M. Holtzman (2009). "Amyloid-{beta} Dynamics Are Regulated by Orexin and the Sleep-Wake Cycle". Science 326 (5955): 1005–7. doi:10.1126/science.1180962. PMC 2789838. PMID 19779148.

15.  ^ Helen Puttick (2006-12-26). "Hope in fight against alcoholism". The Herald.

16.  ^ Lawrence AJ, Cowen MS, Yang HJ, Chen F, Oldfield B (2006). "The orexin system regulates alcohol-seeking in rats". Br. J. Pharmacol. 148 (6): 752–9. doi:10.1038/sj.bjp.0706789. PMC 1617074. PMID 16751790.

17.  ^ Arias-Carrión O, Murillo-Rodriguez E, Xu M, Blanco-Centurion C, Drucker-Colín R, Shiromani PJ (2004). "Transplantation of hypocretin neurons into the pontine reticular formation: preliminary results". Sleep 27 (8): 1465–70. PMC 1201562. PMID 15683135.

18.  ^ "Blocking A Neuropeptide Receptor Decreases Nicotine Addiction". ScienceDaily LLC. 2008-12-01. Retrieved 2009-02-11.

19.  ^ Skrzypski M, T Le T, Kaczmarek P, Pruszynska-Oszmalek E, Pietrzak P, Szczepankiewicz D, Kolodziejski PA, Sassek M, Arafat A, Wiedenmann B, Nowak KW, Strowski MZ (2011 Jul). "Orexin A stimulates glucose uptake, lipid accumulation and adiponectin secretion from 3T3-L1 adipocytes and isolated primary rat adipocytes". Diabetologia 5 (47): 1841–52. PMID 21505958.

20.  ^ Sellayah D, Bharaj P, Sikder D (October 2011). "Orexin is required for brown adipose tissue development, differentiation, and function". Cell Metab. 14 (4): 478–90. doi:10.1016/j.cmet.2011.08.010. PMID 21982708. Lay summary – Orlando Sentinel.

21.  ^ a b Gautvik KM, de Lecea L, et. al. (1996). "Overview of the most prevalent hypothalamus-specific mRNAs, as identified by directional tag PCR subtraction.". PNAS 93 (16): 8733–8738. doi:10.1073/pnas.93.16.8733. PMC 38742. PMID 8710940.

22.  ^ Carl A. Baxter, Ed Cleator, Karel M. J. Brands, John S. Edwards, Robert A. Reamer, Faye J. Sheen, Gavin W. Stewart, Neil A. Strotman, and Debra J. Wallace. (2011). "The First Large-Scale Synthesis of MK-4305: A Dual Orexin Receptor Antagonist for the Treatment of Sleep Disorder.". Organic Process Research and Development 15 (2): 367-375. edit

23.  ^ Acuna-Goycolea C, Li Y, Van Den Pol AN (March 2004). "Group III metabotropic glutamate receptors maintain tonic inhibition of excitatory synaptic input to hypocretin/orexin neurons". J. Neurosci. 24 (12): 3013–22. doi:10.1523/JNEUROSCI.5416-03.2004. PMID 15044540.

24.  ^ Liu ZW, Gao XB (January 2007). "Adenosine inhibits activity of hypocretin/orexin neurons by the A1 receptor in the lateral hypothalamus: a possible sleep-promoting effect". J. Neurophysiol. 97 (1): 837–48. doi:10.1152/jn.00873.2006. PMC 1783688. PMID 17093123.

25.  ^ Ohno K, Hondo M, Sakurai T (March 2008). "Cholinergic regulation of orexin/hypocretin neurons through M(3) muscarinic receptor in mice". J. Pharmacol. Sci. 106 (3): 485–91. doi:10.1254/jphs.FP0071986. PMID 18344611.[dead link]

26.  ^ Muraki Y, Yamanaka A, Tsujino N, Kilduff TS, Goto K, Sakurai T (August 2004). "Serotonergic regulation of the orexin/hypocretin neurons through the 5-HT1A receptor". J. Neurosci. 24 (32): 7159–66. doi:10.1523/JNEUROSCI.1027-04.2004. PMID 15306649.

27.  ^ Fu LY, Acuna-Goycolea C, van den Pol AN (October 2004). "Neuropeptide Y inhibits hypocretin/orexin neurons by multiple presynaptic and postsynaptic mechanisms: tonic depression of the hypothalamic arousal system". J. Neurosci. 24 (40): 8741–51. doi:10.1523/JNEUROSCI.2268-04.2004. PMID 15470140.

28.  ^ Tsujino N, Yamanaka A, Ichiki K, Muraki Y, Kilduff TS, Yagami K, Takahashi S, Goto K, Sakurai T (August 2005). "Cholecystokinin activates orexin/hypocretin neurons through the cholecystokinin A receptor". J. Neurosci. 25 (32): 7459–69. doi:10.1523/JNEUROSCI.1193-05.2005. PMID 16093397.

29.  ^ Li Y, van den Pol AN (January 2005). "Direct and indirect inhibition by catecholamines of hypocretin/orexin neurons". J. Neurosci. 25 (1): 173–83. doi:10.1523/JNEUROSCI.4015-04.2005. PMID 15634779.

30.  ^ Yamanaka A, Muraki Y, Ichiki K, Tsujino N, Kilduff TS, Goto K, Sakurai T (July 2006). "Orexin neurons are directly and indirectly regulated by catecholamines in a complex manner". J. Neurophysiol. 96 (1): 284–98. doi:10.1152/jn.01361.2005. PMID 16611835.

31.  ^ Ohno K, Sakurai T (January 2008). "Orexin neuronal circuitry: role in the regulation of sleep and wakefulness". Front Neuroendocrinol 29 (1): 70–87. doi:10.1016/j.yfrne.2007.08.001. PMID 17910982.

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