Inhibitory and excitatory effects of histamine on suprachiasmatic neurons in rat hypothalamic slice preparation

Liou, Shyh Yuh; Shibata, Shigenobu; Yamakawa, Katsunori; Ueki, Showa

doi:10.1016/0304-3940(83)90231-8

Cited by 42 publications

(5 citation statements)

References 13 publications

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“…A variety of evidence indicates that histamine is a potent regulator of the phase of the circadian system. Prior work has shown that histamine application onto SCN neurons in the rat and hamster hypothalamic slices increases or decreases the electrical activities of these cells [ 64 – 66 ] while bath-applied histamine phase-shifts the circadian neural activity rhythms recorded in hamster and mouse SCN slices [ 6 , 7 , 27 ]. The inhibition of histamine synthesis by α-fluoromethylhistidine decreases the phase shifts of circadian activity rhythms induced by light in the hamster [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

Histamine 1 receptor-Gβγ-cAMP/PKA-CFTR pathway mediates the histamine-induced resetting of the suprachiasmatic circadian clock

Kim

et al. 2016

Mol Brain

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BackgroundRecent evidence indicates that histamine, acting on histamine 1 receptor (H1R), resets the circadian clock in the mouse suprachiasmatic nucleus (SCN) by increasing intracellular Ca2+ concentration ([Ca2+]i) through the activation of CaV1.3 L-type Ca2+ channels and Ca2+-induced Ca2+ release from ryanodine receptor-mediated internal stores.ResultsIn the current study, we explored the underlying mechanisms with various techniques including Ca2+- and Cl−-imaging and extracellular single-unit recording. Our hypothesis was that histamine causes Cl− efflux through cystic fibrosis transmembrane conductance regulator (CFTR) to elicit membrane depolarization needed for the activation of CaV1.3 Ca2+ channels in SCN neurons. We found that histamine elicited Cl− efflux and increased [Ca2+]i in dissociated mouse SCN cells. Both of these events were suppressed by bumetanide [Na+-K+-2Cl− cotransporter isotype 1 (NKCC1) blocker], CFTRinh-172 (CFTR inhibitor), gallein (Gβγ protein inhibitor) and H89 [protein kinase A (PKA) inhibitor]. By itself, H1R activation with 2-pyridylethylamine increased the level of cAMP in the SCN and this regulation was prevented by gallein. Finally, histamine-evoked phase shifts of the circadian neural activity rhythm in the mouse SCN slice were blocked by bumetanide, CFTRinh-172, gallein or H89 and were not observed in NKCC1 or CFTR KO mice.ConclusionsTaken together, these results indicate that histamine recruits the H1R-Gβγ-cAMP/PKA pathway in the SCN neurons to activate CaV1.3 channels through CFTR-mediated Cl− efflux and ultimately to phase-shift the circadian clock. This pathway and NKCC1 may well be potential targets for agents designed to treat problems resulting from the disturbance of the circadian system.

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Section: Discussionmentioning

confidence: 99%

Histamine 1 receptor-Gβγ-cAMP/PKA-CFTR pathway mediates the histamine-induced resetting of the suprachiasmatic circadian clock

Kim

et al. 2016

Mol Brain

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“…In the hypothalamus, HRH2 and other histamine receptors regulate circadian rhythms and feeding behavior ( 122 ). Alternatively, agonism of HRH1 in rodents, an excitatory receptor in contrast to HRH2 ( 123 ), reduces food consumption by ∼50% ( 124 ), while a genetic knockout of HRH1 both increases feeding and disrupts circadian feeding behavior ( 125 ). Data on HRH2 are sparse in comparison to those on HRH1 ( 126 ), but agonism of HRH2 did not significantly affect rodent feeding behavior ( 124 ) and mice HRH2 knockouts reduce nocturnal mice activity ( 126 ).…”

Section: Discussionmentioning

confidence: 99%

Seasonal and comparative evidence of adaptive gene expression in mammalian brain size plasticity

Thomas,

Richter,

O’Neil

et al. 2024

Preprint

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Contrasting almost all other mammalian wintering strategies, Eurasian common shrews,Sorex araneus, endure winter by shrinking their brain, skull, and most organs, only to then regrow to breeding size the following spring. How such tiny mammals achieve this unique brain size plasticity while maintaining activity through the winter remains unknown. To discover potential adaptations underlying this trait, we analyzed seasonal differential expression in the shrew hypothalamus, a brain region that both regulates metabolic homeostasis and drastically changes size and compared hypothalamus expression across species. We discovered seasonal variation in suites of genes involved in energy homeostasis and apoptosis, shrew-specific upregulation of genes involved in the development of the hypothalamic blood brain barrier and calcium signaling, as well as overlapping seasonal and comparative gene expression divergence in genes implicated in the development and progression of human neurological and metabolic disorders, includingCCDC22,FAM57B, andGPR3. With high metabolic rates and facing harsh winter conditions,Sorex araneushave evolved both adaptive and plastic mechanisms to sense and regulate its energy budget. Many of these expression changes mirrored those identified in human neurological and metabolic disease, highlighting the interactions between metabolic homeostasis, brain size plasticity, and longevity.

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“…The SCN is the master circadian pacemaker in the mammalian brain, and sends dense axonal outputs to the SPZ, which negatively regulates aggression via the VMHvl 41 . The HA TMN also projects to the SCN 23,42 and has an inhibitory effect on SCN neuronal activity through H 1 and H 2 receptor activation [43][44][45] . Additional projection mapping and chemogenetic activation studies are required to clarify the contributions of these pathways to territorial aggression induced by HA TMN neuron excitation.…”

Section: Discussionmentioning

confidence: 99%

Chemogenetic modulation of histaminergic neurons in the tuberomammillary nucleus alters territorial aggression and wakefulness

Naganuma

Nakamura

Kuroyanagi

et al. 2021

Preprint

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Designer receptor activated by designer drugs (DREADDs) techniques are widely used to modulate the activities of specific neuronal populations during behavioural tasks. However, DREADDs-induced modulation of histaminergic neurons in the tuberomammillary nucleus (HATMN neurons) has produced inconsistent effects on the sleep–wake cycle, possibly due to the use of Hdc-Cre mice driving Cre recombinase and DREADDs activity outside the targeted region. Moreover, previous DREADDs studies have not examined locomotor activity and aggressive behaviours, which are also regulated by brain histamine levels. In the present study, we investigated the effects of HATMN activation and inhibition on the locomotor activity, aggressive behaviours and sleep–wake cycle of Hdc-Cre mice with minimal non-target expression of Cre-recombinase. Chemoactivation of HATMN moderately enhanced locomotor activity in a novel open field. Activation of HATMN neurons significantly enhanced aggressive behaviour in the resident–intruder test. Wakefulness was increased and non-rapid eye movement (NREM) sleep decreased for an hour by HATMN chemoactivation. Conversely HATMN chemoinhibition decreased wakefulness and increased NREM sleep for 6 hours. These changes in wakefulness induced by HATMN modulation were related to vigilance status transition. These results indicate the influences of HATMN neurons on exploratory activity, territorial aggression, and wake maintenance.

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Inhibitory and excitatory effects of histamine on suprachiasmatic neurons in rat hypothalamic slice preparation

Cited by 42 publications

References 13 publications

Histamine 1 receptor-Gβγ-cAMP/PKA-CFTR pathway mediates the histamine-induced resetting of the suprachiasmatic circadian clock

Histamine 1 receptor-Gβγ-cAMP/PKA-CFTR pathway mediates the histamine-induced resetting of the suprachiasmatic circadian clock

Seasonal and comparative evidence of adaptive gene expression in mammalian brain size plasticity

Chemogenetic modulation of histaminergic neurons in the tuberomammillary nucleus alters territorial aggression and wakefulness

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