Effects of histamine and α-fluoromethylhistidine injections on circadian phase of free-running rhythms

Itowi, Nobuko; Yamatodani, Atsushi; Nonomura, Katsuya; Nakagawa, Hachiro; Wada, Hiroshi

doi:10.1016/0031-9384(90)90125-n

Cited by 34 publications

(14 citation statements)

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“…In experiments performed in free-running conditions in constant darkness, the animals followed their internal rhythm without entrainment by light or other external cues. In terms of this condition, it is reported that histamine is involved in phase shifts of circadian activity [8]. Present results, however, showed that the H1 receptor Values are mean ± SE in 9-week-old mice.…”

Section: Discussioncontrasting

confidence: 53%

“…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%

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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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Section: Discussioncontrasting

confidence: 53%

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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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“…These results are similar to our previous report (Cote and Harrington, 1993) where bath-applied histamine at ZT 14 induced phase delays. Therefore, our results, along with in vivo studies of intraventricular injections of histamine (Itowi et al, 1990), confirm that the magnitude and direction of the phase-shifting effects of histamine depend on circadian phase in a manner similar to light. This pattern of phase shifts is similar to that for glutamate applications to the rat (Ding et al, 1994;Shirakawa and Moore, 1994a) and hamster (Biello et al, 1997) SCN in vitro.…”

Section: Discussionsupporting

confidence: 79%

“…While the photic phase-shifting pattern can be mimicked in vivo by micro-injection of NMDA into the SCN (Mintz and Albers, 1997), a similar pattern is also produced by intraventricular injections of histamine (Itowi et al, 1990). Histamine is a neurotransmitter implicated in the control of sleep and arousal (Sherin et al, 1996;Wada et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Histamine Phase Shifts the Hamster Circadian Pacemaker via an NMDA Dependent Mechanism

1998

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The SCN acts as the central pacemaker for circadian rhythms in mammals. Histamine has been shown to affect circadian rhythms both in vivo and in vitro. We investigated the mechanism by which histamine phase shifts circadian rhythms in vitro. Hypothalamic slices containing the SCN were prepared from golden hamsters, and spontaneous firing rates of individual cells were recorded on the second day in vitro. Application of histamine (1 microM-10 mM) at the extrapolated time of 2 h after lights off (ZT 14) on day 1 in vitro delayed the time of peak firing in a dose-dependent manner. Pre-exposure to the N-methyl-D-aspartate (NMDA) receptor antagonist (+/-)-2-amino-5-phosphonopentanoic acid (AP-5; 100 microM-1 mM) 5 min before histamine (1 microM) was applied to the slice blocked the phase-delaying effects of histamine. Application of the H1 blocker mepryamine (100 nM) or the H2 blocker cimetidine (10 microM) followed by histamine had no effect on the phase delay induced by histamine. In whole cell recordings from acutely dissociated neurons of hamster SCN, histamine (50 microM) was shown to potentiate NMDA-evoked currents by 52 +/- 12%. These experiments demonstrate that histamine phase shifts of the circadian clock are dependent on NMDA receptor activation and that histamine can directly potentiate NMDA currents in SCN neurons. Histamine may alter circadian clock function by acting directly on NMDA receptors, possibly via binding to the polyamine site.

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“…Conflicting observations have also been presented for the excitatory amino acid glutamate, which has been reported to cause dark-pulse type phase shifts in behaving animals (Meijer et al, 1988b) but light-pulse type phase shifts in vitro (Ding et al, 1994). Light-pulse type phase shifting has also been described for histaminergic stimulation (Itowi et al, 1990;Cote and Harrington, 1993) and for the neuropeptide gastrin-releasing peptide (GRP), presented either alone (Piggins et al, 1994) or as part of a multi-peptide "cocktail" (Albers et al, 1991). In addition, these same neurotransmitter systems modulate the circadian pacemaker's cellular and physiological response to light (Liou et al, 1986;Keefe et al, 1987;Ralph and Menaker, 1989;Abe et al, 1992;Colwell and Menaker, 1992;Vindlacheruvu et al, 1992).…”

Section: Introductionmentioning

confidence: 96%

Circadian phase shifting induced by clonidine injections in Syrian hamsters

Rosenwasser

Vogt

Pellowski

1995

Biological Rhythm Research

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The mammalian circadian pacemaker can be phase shifted by photic, pharmacological, and behaviorally-derived stimuli. The phase-response curves (PRCs) characterizing these diverse stimuli may comprise two distinct families; a photic PRC typified by the response to brief light pulses, and a nonphotic PRC, typified by the response to dark pulses and to behavioral activation. The present study examined the phase shifting effects of acute systemic treatment with the alpha2-adrenoceptor agonist, clonidine, in Syrian hamsters. Clonidine injections (0.25 mg/kg, ip) delivered during subjective night mimicked the phase shifting effects of light pulses in animals housed in both constant darkness (DD) and constant red light (RR), but similar effects were not seen in saline-treated controls. Both clonidine and saline injections resulted in phase advances during subjective day, but only in RRhoused animals. Clonidine-induced phase shifting was dose-dependent, but rather high doses were required to induce phase shifts. Pretreatment with the selective noradrenergic neurotoxin, DSP-4, blocked clonidine-induced phase shifting. These results suggest that clonidine acts at presynaptic alpha2-adrenergic autoreceptors to disinhibit spontaneous and/or evoked activity in the photic entrainment pathway.

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Effects of histamine and α-fluoromethylhistidine injections on circadian phase of free-running rhythms

Cited by 34 publications

References 35 publications

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

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

Histamine Phase Shifts the Hamster Circadian Pacemaker via an NMDA Dependent Mechanism

Circadian phase shifting induced by clonidine injections in Syrian hamsters

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