Spinal orexin-1 receptors mediate anti-hyperalgesic effects of intrathecally-administered orexins in diabetic neuropathic pain model rats

Kajiyama, Seiji; Kawamoto, Masashi; Shiraishi, Seiji; Gaus, Syafruddin; Matsunaga, Aki; Suyama, Hidemichi; Yuge, Osafumi

doi:10.1016/j.brainres.2005.03.007

Cited by 65 publications

(47 citation statements)

References 33 publications

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“…Behavioral studies show that Hcrt-1 is analgesic when given i.c.v. or i.v., but not s.c., in mouse and rat models of nociception and hyperalgesia (8)(9)(10). The efficacy of Hcrt-1 was similar to that of morphine in the hotplate test and the carrageenan-induced thermal hyperalgesia test.…”

Section: Dendrites (mentioning

confidence: 78%

“…The efficacy of Hcrt-1 was similar to that of morphine in the hotplate test and the carrageenan-induced thermal hyperalgesia test. Hcrt-1-induced analgesic effects were confirmed, and involvement of the opiate system was ruled out because Hcrt-1 analgesia was blocked by the Hcrt receptor (HcrtR) antagonist SB-334867 but not by naloxone (8)(9)(10). HcrtR antagonists had no effect in baseline acute nociceptive tests but, under inflammatory conditions, were prohyperalgesic, suggesting a tonic inhibitory Hcrt drive under these conditions (8).…”

Section: Dendrites (mentioning

confidence: 99%

“…However, the Hcrt system has also been implicated in nociception, the stress response, and SIA. The Hcrt-1 peptide is analgesic (8)(9)(10), CRF excites Hcrt cells through the CRF receptor 1 (11), and SIA is reduced in Hcrtnull mutant mice (12).…”

Section: Introductionmentioning

confidence: 99%

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Hypocretin/orexin and nociceptin/orphanin FQ coordinately regulate analgesia in a mouse model of stress-induced analgesia

Xie

Wisor²,

Hara³

et al. 2008

J. Clin. Invest.

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Section: Dendrites (mentioning

confidence: 78%

Section: Dendrites (mentioning

confidence: 99%

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Hypocretin/orexin and nociceptin/orphanin FQ coordinately regulate analgesia in a mouse model of stress-induced analgesia

Xie

Wisor²,

Hara³

et al. 2008

J. Clin. Invest.

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“…Spinally applied orexin-A has been shown to induce antinociceptive effects through activation of spinal OX 1 receptors in diabetic rats (19) and carrageenan-treated rats (9). The precise synaptic location of these OX 1 receptors in the context of spinal nociceptive and/or antinociceptive neural transmission remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Role of orexin receptor subtypes in the inhibitory effects of orexin-A on potassium chloride-induced increases in intracellular calcium ion levels in neurons derived from dorsal root ganglion of carrageenan-treated rats

2017

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“…Finally the selectivity of some of the early small molecule orexin antagonists may not be sufficient to provide confirmation of mechanism of action and new more selective pharmacologic tools will probably be required to provide definitive data [64]. This having been said in non-clinical studies, OX-1R has been localized to the spinal cord and dorsal root ganglion [65].OX-A and OX-B have been shown to be analgesic when given i.c.v. and intrathecally but not subcutaneously in line with their peptidic nature [66].…”

mentioning

confidence: 99%

Erratum to: Why does Sleep Stop Migraine?

Bigal¹,

Hargreaves

2014

Curr Pain Headache Rep

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The section titled Subcortical Structures Relevant to Migraine involved in Sleep should read as follows:Our comprehension of the physiology of the daily cycles of sleep and wakefulness, as well as the neuronal circuitry and molecular basis of the biological clock that underpins human circadian rhythms (daily sleep-wake cycles), has increased substantially in recent years.The wake promotion systems and the sleep promotion system are temporally controlled by the endogenous circadian pacemaker contained within the suprachiasmatic nuclei (SCN) that functions autonomously as the brain's master clock. The SCN receives information about light and dark periods from melanopsin expressing retinal ganglion cells during the day (the light entrainment system) and melatonin from the pineal gland at night to reset the human 24.5 hour circadian rhythm to our 24 hour day length. The molecular basis of the clock function involves transcriptional and translational regulation of the expression of genes such as period, clock, Bmal and cryptochrome that when mutated or deleted disrupt circadian rhythm cycles [49].Daily oscillations in SCN activity signal through the subparaventricular zone and the dorsal medial hypothalamus to both GABA-ergic neurons of the ventrolateral pre-optic area of the hypothalamus (VLPO) and the wake promoting orexinergic neurons of the lateral hypothalamus. GABA-ergic neurons promote sleep by sending inhibitory projections both to orexin neurons as well as brain stem nuclei such as locus ceruleus (norepinephrine), Raphe nucleus (serotonin) and tuberomamillary nucleus (histamine) that together with cholinergic projections from the basal forebrain form the ascending arousal systems. Attenuation of this inhibitory signal and increased excitatory input from the SCN to orexin secreting neurons that innervate these monoaminergic brain stem arousal nuclei promotes waking and somatosensory function. [50]. Increasing evidence suggests that human circadian rhythms are regulated by a thalamic switch that can be activated or deactivated to regulate sensory information reaching the cerebral cortex and the degree of consciousness [51]. The transition from sleep to wakefulness comes as thalamocortical pathways activate the cortex that has been primed by neurotransmitters (serotonin, histamine, norepinephrine) released from ascending pathways originating in the brain stem. The extent of information passing to the cortex through the thalamus is "gated" based on the arousal level of the central nervous system that is in turn set by outputs from the reticulo-activating systems (RAS) of the brain stem and hypothalamus.Migraine is often triggered by stimuli that activate the RAS such as environmental stimuli, exercise, changes in levels of stress, fatigue, sleep deprivation or poor sleep hygiene [52,53] suggesting that the propensity to sleep during migraine could be an endogenous homeostatic response that can reduce the intensity or frequency of migraine headaches. The mechanisms through which physiological sleep achieves an an...

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Spinal orexin-1 receptors mediate anti-hyperalgesic effects of intrathecally-administered orexins in diabetic neuropathic pain model rats

Cited by 65 publications

References 33 publications

Hypocretin/orexin and nociceptin/orphanin FQ coordinately regulate analgesia in a mouse model of stress-induced analgesia

Hypocretin/orexin and nociceptin/orphanin FQ coordinately regulate analgesia in a mouse model of stress-induced analgesia

Role of orexin receptor subtypes in the inhibitory effects of orexin-A on potassium chloride-induced increases in intracellular calcium ion levels in neurons derived from dorsal root ganglion of carrageenan-treated rats

Erratum to: Why does Sleep Stop Migraine?

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