Effect of histamine depletion on the circadian amplitude of the sleep-wakefulness cycle

Itowi, Nobuko; Yamatodani, Atsushi; Kiyono, S; Hiraiwa, M.; Wada, Hiroshi

doi:10.1016/0031-9384(91)90293-w

Cited by 30 publications

(12 citation statements)

References 16 publications

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“…However, inactivation of the histamine system via lesions (302, 413), knockout of the histamine H 1 receptor (528), administration of an irreversible inhibitor of the histamine synthesizing enzyme histidine decarboxylase (HDC; Refs. 551, 642, 1152) or knockout of HDC (29, 978) have relatively minor effects on 24-h amounts of waking or cortical activation suggesting that, similar to the other aminergic systems, the histamine system is not absolutely essential for wakefulness. Histamine neurons maintain their level of firing during cataplectic attacks in narcoleptic animals (in contrast to norepinephrine and serotonin neurons) implicating them in the preservation of consciousness which accompanies the cataplectic state (564).…”

Section: Wakefulnessmentioning

confidence: 99%

Control of Sleep and Wakefulness

Brown

Basheer

Mckenna

et al. 2012

Physiological Reviews

1,198

1,105

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This review summarizes the brain mechanisms controlling sleep and wakefulness. Wakefulness promoting systems cause low-voltage, fast activity in the electroencephalogram (EEG). Multiple interacting neurotransmitter systems in the brain stem, hypothalamus, and basal forebrain converge onto common effector systems in the thalamus and cortex. Sleep results from the inhibition of wake-promoting systems by homeostatic sleep factors such as adenosine and nitric oxide and GABAergic neurons in the preoptic area of the hypothalamus, resulting in large-amplitude, slow EEG oscillations. Local, activity-dependent factors modulate the amplitude and frequency of cortical slow oscillations. Non-rapid-eye-movement (NREM) sleep results in conservation of brain energy and facilitates memory consolidation through the modulation of synaptic weights. Rapid-eye-movement (REM) sleep results from the interaction of brain stem cholinergic, aminergic, and GABAergic neurons which control the activity of glutamatergic reticular formation neurons leading to REM sleep phenomena such as muscle atonia, REMs, dreaming, and cortical activation. Strong activation of limbic regions during REM sleep suggests a role in regulation of emotion. Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function. Sleep disruption interferes with the normal restorative functions of NREM and REM sleep, resulting in disruptions of breathing and cardiovascular function, changes in emotional reactivity, and cognitive impairments in attention, memory, and decision making.

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Section: Wakefulnessmentioning

confidence: 99%

Control of Sleep and Wakefulness

Brown

Basheer

Mckenna

et al. 2012

Physiological Reviews

1,198

1,105

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“…It is especially important that the hypothalamus, which plays a role in the regulation of the autonomic nervous system, responds to the environmental factors. Histaminergic neurons modulate many physiological functions, such as the arousal state [2,3], locomotor activity [4], feeding and drinking [5,6], lipid metabolism [7], and circadian rhythm [8,9]. These functions are closely related to changes in ventilation and are predominantly mediated by histamine type-1 (H1) receptors rather than type-2 (H2) receptors.…”

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confidence: 99%

Contribution of Histamine Type-1 Receptor to Metabolic and Behavioral Control of Ventilation

et al. 2006

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Histaminergic neurons in the hypothalamus are well documented as being involved in the control of autonomic functions, such as the balance of energy metabolism and circadian rhythm. We tested the hypothesis that an activation of the histamine type-1 (H1) receptor is required for the control of ventilation during the course of a day in free-moving mice. Ventilation, aerobic metabolism, and electroencephalogram were measured by a whole-body-plethysmograph, a magnetic-type mass spectrometry system, and a telemetry system, respectively, in H1 receptor-knockout (H1RKO) and wild-type mice. Both genotypes showed daily oscillations in minute ventilation ( E ) and oxygen consumption ( o 2 ), with greater values during the dark period compared to the light period. In the latter, H1RKO mice showed increased E and CO 2 excretion ( co 2 ) relative to wild-type mice, and E was comparable to the co 2 increase. However, there was no change in o 2 in H1RKO mice, suggesting that differences in co 2 between genotypes are responsible for differences in E during the light period. During the dark period, co 2 was elevated in H1RKO mice compared with WT mice. Because there was no difference in E , the ratio of E to co 2 was reduced in H1RKO mice. Electroencephalogram results suggested that this might be due to a depressed arousal state in H1RKO mice because the ratio of delta to theta band power spectrum densities was greater in H1RKO mice than in wild-type mice. We concluded that histamine modulates ventilation by affecting metabolism and arousal state via H1 receptors.Key words: histamine type-1 receptor, metabolism, circadian pattern, arousal state, mice.The respiratory pattern is generated by the intrinsic cellular mechanisms and the network system of the respiratory neuron in the lower brain stem, which is affected by metabolic and behavioral control systems. During both awake and sleep stages, the metabolic control of respiration is always activated. However, in the awake stage respiration is influenced by various intrinsic or extrinsic environmental factors, such as thermal stress, pain, and various emotional changes. These behavioral controls are believed to be generated in the higher center rather than in the brain stem [1]. It is especially important that the hypothalamus, which plays a role in the regulation of the autonomic nervous system, responds to the environmental factors. Histaminergic neurons modulate many physiological functions, such as the arousal state [2,3], locomotor activity [4], feeding and drinking [5,6], lipid metabolism [7], and circadian rhythm [8,9]. These functions are closely related to changes in ventilation and are predominantly mediated by histamine type-1 (H1) receptors rather than type-2 (H2) receptors. To date, postsynaptic H1 and H2 receptors and presynaptic type-3 autoreceptors, have been identified in the brain [10]. Histaminergic neuronal cell bodies are located in the tuberomammillary nucleus of the posterior hypothalamus and project ascending and descending axons to much of the b...

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“…On the other hand, Kiyono et al 17) and Itowi et al 18) reported that a-fluoromethylhistidine (a-FMH), a specific inhibitor of histidine decarboxylase, decreased the awake time and increased slow wave sleep time during the dark period, whereas a-FMH showed no effect on the awake time and slow wave sleep time during the light period in rats. Mochizuki et al 19) and Chu et al 20) also demonstrated a clear circadian rhythm of histamine release from the anterior hypothalamus or the frontal cortex, that is, histamine release during the dark period, awake episodes, was significant higher than during the light period, sleep episodes, in rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of Histamine H1-Antagonists on Sleep-Awake State in Rats Placed on a Grid Suspended over Water or on Sawdust

Tokunaga

Tsutsui

Obara

et al. 2009

Biological & Pharmaceutical Bulletin

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The present study was performed to investigate the effects of histamine H 1 -antagonists on the sleep-awake state in rats placed on a grid suspended over water in comparison with rats placed on sawdust. When rats were placed on the grid suspended over water, significant increases in the awake time and decreases in non-rapid eye movement (non-REM) sleep time were observed compared with in rats on sawdust, even when measured hourly for 6 h. Diphenhydramine, chlorpheniramine and promethazine caused a significant decrease in the awake time and increase in non-REM sleep time in rats placed on the grid suspended over water for 1-2 h and/or 2-3 h after administration. On the other hand, in rats placed on sawdust, no significant differences were observed in the awake time and non-REM sleep time with diphenhydramine and chlorpheniramine compared with the control. Different from these two drugs, promethazine caused a significant decrease in the awake time and increase in non-REM sleep time 1-2 h and 2-3 h after administration even when rats were placed on sawdust at a relatively high dose. These results clearly indicate that histamine H 1 -antagonists had potent effects on decreasing the awake time and increasing non-REM sleep time under the conditions of an activated histaminergic system.

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Effect of histamine depletion on the circadian amplitude of the sleep-wakefulness cycle

Cited by 30 publications

References 16 publications

Control of Sleep and Wakefulness

Control of Sleep and Wakefulness

Contribution of Histamine Type-1 Receptor to Metabolic and Behavioral Control of Ventilation

Effects of Histamine H1-Antagonists on Sleep-Awake State in Rats Placed on a Grid Suspended over Water or on Sawdust

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