Circadian rhythm photic phase shifts are not altered by histamine receptor antagonists

Eaton, Sara J.; Eoh, Sun; Meyer, Jen; Hoque, Sabina; Harrington, Mary E.

doi:10.1016/s0361-9230(96)00179-7

Cited by 12 publications

(4 citation statements)

References 19 publications

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“…Therefore, we examined the effect of mepyramine, a high affinity (K d ~ 0.8 nM; Hill, 1992) H1 antagonist, on the histamine-induced phase shift. This conclusion is consistent with our results from in vivo studies in which H1 receptor antagonists had no effect on lightinduced phase shifts (Eaton et al, 1996). However, at a more reasonable dose (100 nM) at which mepyramine is less likely to have nonspecific effects (Hill, 1992), the histamine-induced phase delay persisted.…”

Section: Discussionsupporting

confidence: 91%

“…In vivo studies have also shown that depletion of brain histamine levels by inhibition of histamine synthesis reduces light-pulseinduced phase shifts in circadian rhythms of hamster wheel-running activity (Eaton et al, 1995). Histamine does not appear to induce this effect through any of the three major histamine receptor subtypes, H1, H2, or H3 (Eaton et al, 1996) despite the large number of H1 binding sites found in the rat SCN (Palacios et al, 1981). The histamine-induced photic phase-shifting pattern has also been demonstrated in vitro using the hamster SCN brain slice preparation (Cote and Harrington, 1993).…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

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

1998

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“…It is also reported that at the level of the SCN the direct excitatory effects of histamine on neuronal firing is mediated via H 1 receptors and the inhibitory effects via H 2 receptors [ 82 , 83 ]. However, in vivo studies, it has been shown that the effects of histamine on circadian rhythms may be mediated through receptors other than histamine receptors [ 84 , 85 ]. The foregoing discussion supports the view that histamine may exert modifying effects on circadian rhythmicity as well as neuronal excitability.…”

Section: Retinohypothalamic Tract (Rht) and Its Neurotransmittersmentioning

confidence: 99%

Neurotransmitters of the suprachiasmatic nuclei

Reghunandanan¹,

Reghunandanan²

2006

J Circadian Rhythms

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There has been extensive research in the recent past looking into the molecular basis and mechanisms of the biological clock, situated in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus. Neurotransmitters are a very important component of SCN function. Thorough knowledge of neurotransmitters is not only essential for the understanding of the clock but also for the successful manipulation of the clock with experimental chemicals and therapeutical drugs. This article reviews the current knowledge about neurotransmitters in the SCN, including neurotransmitters that have been identified only recently. An attempt was made to describe the neurotransmitters and hormonal/diffusible signals of the SCN efference, which are necessary for the master clock to exert its overt function. The expression of robust circadian rhythms depends on the integrity of the biological clock and on the integration of thousands of individual cellular clocks found in the clock. Neurotransmitters are required at all levels, at the input, in the clock itself, and in its efferent output for the normal function of the clock. The relationship between neurotransmitter function and gene expression is also discussed because clock gene transcription forms the molecular basis of the clock and its working.

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“…The role of Hrh2 in circadian regulation should be discussed although this was not addressed in the current study. Pharmacological inhibition of Hrh2 by cimetidine was reported to lead to occasional potentiation of the effect of histamine on SCN neurons in rat brain slice preparations [ 31 , 32 ], but this treatment did not cause any phase shifts, when administered to hamsters [ 38 ]. Similarly, the brain-penetrating Hrh2 antagonist zolantidine had no effect on light-induced phase shift as shown for hamsters, or the lengths or distributions of NREM, REM and wakefulness states as shown on rats [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

On the Role of Histamine Receptors in the Regulation of Circadian Rhythms

2015

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Several lines of evidence suggest a regulatory role of histamine in circadian rhythms, but little is known about signaling pathways that would be involved in such a putative role. The aim of this study was to examine whether histamine mediates its effects on the circadian system through Hrh1 or Hrh3 receptors. We assessed both diurnal and free-running locomotor activity rhythms of Hrh1 -/- and Hrh3 -/- mice. We also determined the expression of Per1, Per2 and Bmal1 genes in the suprachiasmatic nuclei, several areas of the cerebral cortex and striatum under symmetric 24 h light-dark cycle at zeitgeber times 14 and 6 by using radioactive in situ hybridization. We found no differences between Hrh1 -/- and wild type mice in the length, amplitude and mesor of diurnal and free-running activity rhythms as well as in expression of Per1, Per2 and Bmal1 genes in any of the examined brain structures. The amplitude of free-running activity rhythm of the Hrh3 -/- mice was significantly flattened, whereas the expression of the clock genes in Hrh3 -/- mice was similar to the wild type animals in all of the assessed brain structures. Therefore, the knockout of Hrh1 receptor had no effects on the circadian rhythm of spontaneous locomotion, and a knockout of Hrh3 receptor caused a substantial reduction of free-running activity rhythm amplitude, but none of these knockout models affected the expression patterns of the core clock genes in any of the studied brain structures.

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Circadian rhythm photic phase shifts are not altered by histamine receptor antagonists

Cited by 12 publications

References 19 publications

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

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

Neurotransmitters of the suprachiasmatic nuclei

On the Role of Histamine Receptors in the Regulation of Circadian Rhythms

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