Mast cell involvement in glucose tolerance impairment caused by chronic mild stress with sleep disturbance

Chikahisa, Sachiko; Harada, Saki; Shimizu, Noriyuki; Shiuchi, Tetsuya; Otsuka, Airi; Nishino, Seiji; Séi, Hiroyoshi

doi:10.1038/s41598-017-14162-w

Cited by 15 publications

(7 citation statements)

References 24 publications

(26 reference statements)

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“…Histidine decarboxylase is also found in brain‐resident mast cell and microglia (Iida et al, 2015; Silver et al, 1996). Although recent reports have indicated the involvement of mast cells in sleep–wake cycles and glucose homeostasis (Chikahisa et al, 2017; Chikahisa et al, 2013), and the impact of histamine‐dependent microglial control on depression‐like behaviours (Iida et al, 2017), further studies are required to elucidate the roles of histamine released from mast cells and microglia in brain functions.…”

Section: Histamine Receptors Histidine Decarboxylase and Histamine Nmentioning

confidence: 99%

Histaminergic neurons in the tuberomammillary nucleus as a control centre for wakefulness

Yoshikawa

Nakamura

Yanai

2020

British J Pharmacology

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Histamine plays pleiotropic roles as a neurotransmitter in the physiology of brain function, this includes the maintenance of wakefulness, appetite regulation and memory retrieval. Since numerous studies have revealed an association between histaminergic dysfunction and diverse neuropsychiatric disorders, such as Alzheimer's disease and schizophrenia, a large number of compounds acting on the brain histamine system have been developed to treat neurological disorders. In 2016, pitolisant, which was developed as a histamine H3 receptor inverse agonist by Schwartz and colleagues, was launched for the treatment of narcolepsy, emphasising the prominent role of brain histamine on wakefulness. Recent advances in neuroscientific techniques such as chemogenetic and optogenetic approaches have led to remarkable progress in the understanding of histaminergic neural circuits essential for the control of wakefulness. In this review article, we summarise the basic knowledge about the histaminergic nervous system and the mechanisms underlying sleep/wake regulation that are controlled by the brain histamine system. LINKED ARTICLES This article is part of a themed issue on Neurochemistry in Japan. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.4/issuetoc

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Section: Histamine Receptors Histidine Decarboxylase and Histamine Nmentioning

confidence: 99%

Histaminergic neurons in the tuberomammillary nucleus as a control centre for wakefulness

Yoshikawa

Nakamura

Yanai

2020

British J Pharmacology

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“…Mice normally show a strong increase in wake when food deprived, but mice without mast cells lack this response, either due to poor promotion of wake or reduced appetite [41]. In addition, chronic mild stress doubles the number of brain mast cells and increases wake during the active period [42]. Although these observations are intriguing, mice lacking mast cells have normal amounts of wake, NREM, and REM sleep [41], and determining how these cells contribute to normal or pathological sleep/wake behavior will be important directions for future research.…”

Section: Histamine Signaling and Sleep/wake Behaviormentioning

confidence: 99%

Histamine: neural circuits and new medications

Scammell

Jackson

Franks

et al. 2018

Sleep

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Histamine was first identified in the brain about 50 years ago, but only in the last few years have researchers gained an understanding of how it regulates sleep/wake behavior. We provide a translational overview of the histamine system, from basic research to new clinical trials demonstrating the usefulness of drugs that enhance histamine signaling. The tuberomammillary nucleus is the sole neuronal source of histamine in the brain, and like many of the arousal systems, histamine neurons diffusely innervate the cortex, thalamus, and other wake-promoting brain regions. Histamine has generally excitatory effects on target neurons, but paradoxically, histamine neurons may also release the inhibitory neurotransmitter GABA. New research demonstrates that activity in histamine neurons is essential for normal wakefulness, especially at specific circadian phases, and reducing activity in these neurons can produce sedation. The number of histamine neurons is increased in narcolepsy, but whether this affects brain levels of histamine is controversial. Of clinical importance, new compounds are becoming available that enhance histamine signaling, and clinical trials show that these medications reduce sleepiness and cataplexy in narcolepsy.

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“…Several inflammatory conditions are worsened by stress, and mast cell activation with inflammatory mediator release plays a crucial role in stress dependent inflammatory mechanism (Theoharides et al, 2004 ). A recent study showed chronic mild stress for 3 weeks increased the number of mast cells in the brain and disturbed sleep in mice (Chikahisa et al, 2017 ). Interaction between hypothalamus, pituitary, and adrenal gland is an important stress response in neuropsychiatric conditions and depression (Anisman and Merali, 2003 ).…”

Section: Stress Mast Cells and Inflammationmentioning

confidence: 99%

Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer's Disease Pathogenesis

et al. 2017

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Mast cells are localized throughout the body and mediate allergic, immune, and inflammatory reactions. They are heterogeneous, tissue-resident, long-lived, and granulated cells. Mast cells increase their numbers in specific site in the body by proliferation, increased recruitment, increased survival, and increased rate of maturation from its progenitors. Mast cells are implicated in brain injuries, neuropsychiatric disorders, stress, neuroinflammation, and neurodegeneration. Brain mast cells are the first responders before microglia in the brain injuries since mast cells can release prestored mediators. Mast cells also can detect amyloid plaque formation during Alzheimer's disease (AD) pathogenesis. Stress conditions activate mast cells to release prestored and newly synthesized inflammatory mediators and induce increased blood-brain barrier permeability, recruitment of immune and inflammatory cells into the brain and neuroinflammation. Stress induces the release of corticotropin-releasing hormone (CRH) from paraventricular nucleus of hypothalamus and mast cells. CRH activates glial cells and mast cells through CRH receptors and releases neuroinflammatory mediators. Stress also increases proinflammatory mediator release in the peripheral systems that can induce and augment neuroinflammation. Post-traumatic stress disorder (PTSD) is a traumatic-chronic stress related mental dysfunction. Currently there is no specific therapy to treat PTSD since its disease mechanisms are not yet clearly understood. Moreover, recent reports indicate that PTSD could induce and augment neuroinflammation and neurodegeneration in the pathogenesis of neurodegenerative diseases. Mast cells play a crucial role in the peripheral inflammation as well as in neuroinflammation due to brain injuries, stress, depression, and PTSD. Therefore, mast cells activation in brain injury, stress, and PTSD may accelerate the pathogenesis of neuroinflammatory and neurodegenerative diseases including AD. This review focusses on how mast cells in brain injuries, stress, and PTSD may promote the pathogenesis of AD. We suggest that inhibition of mast cells activation and brain cells associated inflammatory pathways in the brain injuries, stress, and PTSD can be explored as a new therapeutic target to delay or prevent the pathogenesis and severity of AD.

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Mast cell involvement in glucose tolerance impairment caused by chronic mild stress with sleep disturbance

Cited by 15 publications

References 24 publications

Histaminergic neurons in the tuberomammillary nucleus as a control centre for wakefulness

Histaminergic neurons in the tuberomammillary nucleus as a control centre for wakefulness

Histamine: neural circuits and new medications

Mast Cell Activation in Brain Injury, Stress, and Post-traumatic Stress Disorder and Alzheimer's Disease Pathogenesis

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