Effects of selective activation or blockade of the histamine H3 receptor on sleep and wakefulness

Monti, Jaime M.; Jantos, Héctor; Boussard, M.; Altier, H.; Orellana, Carmen; Olivera, Silvia Leonor

doi:10.1016/0014-2999(91)90911-9

Cited by 90 publications

(18 citation statements)

References 16 publications

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“…These results suggest that the cortical activation induced via the inhibition of the H3-receptor by ciproxifan is able to oppose the active induction of sleep by light early in the dark period. This is consistent with results from other studies showing that the inhibition of the H3-receptor is sufficient to promote wakefulness [34–37]. As expected, no significant changes in total sleep amount were observed during the rest of the dark period post-injection.…”

Section: Discussionsupporting

confidence: 93%

“…The blockade of H3 receptors promotes wakefulness [34–37]. As such, we questioned whether the blockade of H3 receptors by ciproxifan, an H3-receptor antagonist, would be sufficient to block the sleep inducing effects of light in the dark period in WT mice.…”

Section: Resultsmentioning

confidence: 99%

“…An important feature of the histaminergic system is that histamine inhibits its own release and synthesis via the histamine H3 pre-synaptic autoreceptor [29,30]. As such, administration of the histamine H3 receptor antagonists increase the synthesis and release of histamine [29,31–33] resulting in an enhancement of wakefulness and cortical theta rhythms [34–37]. …”

Section: Introductionmentioning

confidence: 99%

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Loss of Melanopsin Photoreception and Antagonism of the Histamine H3 Receptor by Ciproxifan Inhibit Light-Induced Sleep in Mice

et al. 2015

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Light has direct effects on sleep and wakefulness causing arousal in diurnal animals and sleep in nocturnal animals. In the present study, we assessed the modulation of light-induced sleep by melanopsin and the histaminergic system by exposing mice to millisecond light flashes and continuous light respectively. First, we show that the induction of sleep by millisecond light flashes is dose dependent as a function of light flash number. We found that exposure to 60 flashes of light occurring once every 60 seconds for 1-h (120-ms of total light over an hour) induced a similar amount of sleep as a continuous bright light pulse. Secondly, the induction of sleep by millisecond light flashes was attenuated in the absence of melanopsin when animals were presented with flashes occurring every 60 seconds over a 3-h period beginning at ZT13. Lastly, the acute administration of a histamine H3 autoreceptor antagonist, ciproxifan, blocked the induction of sleep by a 1-h continuous light pulse during the dark period. Ciproxifan caused a decrease in NREMS delta power and an increase in theta activity during both sleep and wake periods respectively. The data suggest that some form of temporal integration occurs in response to millisecond light flashes, and that this process requires melanopsin photoreception. Furthermore, the pharmacological data suggest that the increase of histaminergic neurotransmission is sufficient to attenuate the light-induced sleep response during the dark period.

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Section: Discussionsupporting

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Loss of Melanopsin Photoreception and Antagonism of the Histamine H3 Receptor by Ciproxifan Inhibit Light-Induced Sleep in Mice

et al. 2015

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“…Thioperamide (1-4 mg/kg i.p.) increased wakefulness and decreased NREM and REM sleep in rats [139], an effect not seen in H 3 -/mice. In cats, oral administration of thioperamide (2-10 mg/kg) elicited a marked, dose-related increase in waking at the expense of both REM and NREM sleep [51].…”

Section: H 3 Receptor Antagonists and Promotion Of Wakementioning

confidence: 70%

The Prevalence, Morbidities, and Treatments of Insomnia

Zammit

2007

CNSNDDT

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Insomnia is a common condition that often is co-morbid with other illnesses. It is associated with significant morbidities, including nighttime distress, impaired cognitive functioning, impaired daytime functioning, and increased risk of accidents. People with insomnia utilize healthcare services more often than those without insomnia, and they are at greater risk for the development of certain health problems; most notably psychiatric illness such as depression. It is now known that the significant impact of insomnia warrants diagnosis and treatment. Behavioral and psychopharmacological treatments have been available for some time. However, formerly common classes of therapeutics such as the barbiturates and benzodiazepines have been replaced by new allosteric modulators of the GABA(A) receptor and other therapeutics with novel mechanisms of action. This article presents existing approaches to insomnia treatment, and reviews new treatments, therapeutic targets, and treatment approaches to insomnia under development that may offer promise to practitioners and patients.

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“…In contrast, bilateral application of (R) α-methyl-histamine into the TMN region increased NREM sleep with a concomitant decrease in wakefulness and REM sleep suggesting that activation of H 3 receptor in the TMN is likely to block histamine release resulting in reduced wakefulness. The NREM inducing effect of (R) α-methyl-histamine was attenuated if the rats were pretreated with thioperamide (59). …”

Section: Pharmacological Studies In Animalsmentioning

confidence: 99%

Histamine in the regulation of wakefulness

Thakkar

2011

Sleep Medicine Reviews

193

118

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The histaminergic system is exclusively localized within the posterior hypothalamus with projection to almost all the major regions of the central nervous system. Strong and consistent evidence exist to suggest that histamine, acting via H 1 and/or H 3 receptor has a pivotal role in the regulation of sleep-wakefulness. Administration of histamine or H 1 receptor agonists induced wakefulness, whereas administration of H 1 receptor antagonists promoted sleep. The H 3 receptor functions as an auto-receptor and regulates the synthesis and release of histamine. Activation of H 3 receptor decreased histamine release and promoted sleep. Conversely, blockade of H 3 receptor promoted wakefulness. Histamine release in the hypothalamus and other target regions was highest during wakefulness. The histaminergic neurons displayed maximal activity during the state of vigilance, and cease their activity during NREM and REM sleep. The cerebrospinal levels of histamine were reduced in diseased states where hypersomnolence was a major symptom. The histamine deficient HDC KO mice displayed sleep fragmentation and increased REM sleep during the light period along with profound wakefulness deficit at dark onset, and in novel environment. Similar results were obtained when histamine neurons were lesioned. These studies strongly implicate the histaminergic neurons of the TMN to play a critical role in the maintenance of high vigilance state during wakefulness.

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Effects of selective activation or blockade of the histamine H3 receptor on sleep and wakefulness

Cited by 90 publications

References 16 publications

Loss of Melanopsin Photoreception and Antagonism of the Histamine H3 Receptor by Ciproxifan Inhibit Light-Induced Sleep in Mice

Loss of Melanopsin Photoreception and Antagonism of the Histamine H3 Receptor by Ciproxifan Inhibit Light-Induced Sleep in Mice

The Prevalence, Morbidities, and Treatments of Insomnia

Histamine in the regulation of wakefulness

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