Effects of GABA-Mimetic Drugs on Turnover of Histamine in the Mouse Brain

Nishibori, Masahiro; Oishi, Ryozo; Itoh, Yoshinori; Saeki, Kiyomi

doi:10.1254/jjp.41.403

Cited by 10 publications

(3 citation statements)

References 16 publications

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“…Increased GABA release in the PH has been reported during REM sleep (28). Nishibori et al (27) and Oishi et al (31) reported that GABA agonists decreased the turnover of HA in mouse brain. These findings suggest that increased levels of GABA may override any direct effects of glutamate on HA neurons during REM sleep.…”

Section: Discussionmentioning

confidence: 99%

Rapid changes in glutamate levels in the posterior hypothalamus across sleep-wake states in freely behaving rats

John

Ramanathan²,

Siegel³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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John J, Ramanathan L, Siegel JM. Rapid changes in glutamate levels in the posterior hypothalamus across sleep-wake states in freely behaving rats. Am J Physiol Regul Integr Comp Physiol 295: R2041-R2049, 2008. First published September 24, 2008 doi:10.1152/ajpregu.90541.2008The histamine-containing posterior hypothalamic region (PH-TMN) plays a key role in sleep-wake regulation. We investigated rapid changes in glutamate release in the PH-TMN across the sleep-wake cycle with a glutamate biosensor that allows the measurement of glutamate levels at 1-to 4-s resolution. In the PH-TMN, glutamate levels increased in active waking (AW) and rapid eye movement (REM) sleep compared with quiet waking and nonrapid eye movement (NREM) sleep. There was a rapid (0.6 Ϯ 1.8 s) and progressive increase in glutamate levels at REM sleep onset. A reduction in glutamate levels consistently preceded the offset of REM sleep by 8 Ϯ 3 s. Short-duration sleep deprivation resulted in a progressive increase in glutamate levels in the PH-TMN, perifornical-lateral hypothalamus (PF-LH), and cortex. We found that in the PF-LH, glutamate levels took a longer time to return to basal values compared with the time it took for glutamate levels to increase to peak values during AW onset. This is in contrast to other regions we studied in which the return to baseline values after AW was quicker than their rise with waking onset. In summary, we demonstrated an increase in glutamate levels in the PH-TMN with REM/AW onset and a drop in glutamate levels before the offset of REM. High temporal resolution measurement of glutamate levels reveals dynamic changes in release linked to the initiation and termination of REM sleep. rapid eye movement sleep; histamine; microdialysis; biosensor; cortex VARIOUS STUDIES HAVE IMPLICATED glutamatergic mechanisms in the control of sleep-wake states. In vitro experiments reported a differential glutamate release in brain regions of long-sleep and short-sleep mice (11). Glutamate release was higher during wakefulness than during sleep in the pedunculopontine tegmental nucleus (22), whereas enhanced glutamate release during rapid eye movement (REM) sleep was observed in the rostromedial medulla (24). Paradoxical sleep deprivation increased the content of glutamate and glutamine in the rat cerebral cortex (3).Glutamate excites both cortical and subcortical neurons and enhances the in vivo release of histamine (HA) through presynaptic N-methyl-D-aspartate receptors in the anterior hypothalamus of the rat (32). Single cell recording and microdialysis experiments demonstrate that HA cell activity is reduced in nonrapid eye movement (NREM) sleep and REM sleep compared with waking (7,20). We hypothesized that changes in glutamate release in the posterior hypothalamus histaminergic tuberomammillary nucleus (PH-TMN) and in the terminal regions of HA neurons could affect HA release and sleep-wake states. Dysfunction of the Hcrt system produces the sleep disorder narcolepsy (35,38,44). Hcrt neurons contain glutamate as a cotransmit...

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Section: Discussionmentioning

confidence: 99%

Rapid changes in glutamate levels in the posterior hypothalamus across sleep-wake states in freely behaving rats

John

Ramanathan²,

Siegel³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Using a superfusion method, Kishino et al (1989) reported that GABA reduced K + -evoked release of histamine from rat hypothalamic slices, suggesting presynaptic regulation of histamine release. Nishibori et al (1986) and reported that GABA agonists decreased the turnover of histamine in mouse brain. Most of these studies used exogenous GABA or GABA-mimetics.…”

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confidence: 99%

Endogenous GABA Modulates Histamine Release from the Anterior Hypothalamus of the Rat

Okakura-Mochizuki

Mochizuki

Yamamoto³

et al. 1996

Journal of Neurochemistry

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Using a microdialysis method, we investigated the effects of the nipecotic acid-induced increase in content of endogenous GABA on in vivo release of histamine from the anterior hypothalamus (AHy) of urethane-anesthetized rats. Nipecotic acid (0.5 mM), an inhibitor of GABA uptake, decreased histamine release to -~60%of the basal level. This effect was partially antagonized by picrotoxin (0.1 mM), an antagonist of GABAA receptors, or phaclofen (0.1 mM), an antagonist of GABAB receptors. These results suggest that histamine release is modulated by endogenous GABA through both GABAA and GABAB receptors. When the tuberomammillary nucleus, where the cell bodies of the histaminergic neurons are localized, was stimulated electrically, the evoked release of histamine from the nerve terminals in the AHy was significantly enhanced by phaclofen, suggesting that GABAB receptors may be located on the histaminergic nerve terminals and modulate histamine release presynaptically. On the other hand, picrotoxin caused an increase in histamine release to~-~1 70% of the basal level, and this increase was diminished by coinfusion with -) -2-amino-5-phosphonopentanoic acid (0.1 mM), an antagonist of NMDA receptors. Previously, we demonstrated tonic control of histamine release by glutamate mediated through NMDA receptors located on the histaminergic terminals in the AHy. These results suggest the possible localization of GABAA receptors on glutamatergic nerve terminals and that the receptors may regulate the basal release of histamine indirectly.

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“…Muscimol, a GABA A receptor agonist, decreases histamine turnover in the mouse brain [415]. Histamine turnover in the brain is also rapidly reduced after administration of GABAergic sedative drugs such as barbiturates and benzodiazepines [398,416], presumably as a result of their interaction with GABA A receptors present on histaminergic neurons [369].…”

Section: Physiological Changesmentioning

confidence: 99%

Neuropharmacology of Histamine in Brain

Faucard

Schwartz

2007

Handbook of Contemporary Neuropharmacology

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Histamine is an important neurotransmitter in brain. Histaminergic neurons emanating from the tuberomamillary nucleus in the hypothalamus project diffusely to the whole brain. Histamine acts via stimulation of three receptor subtypes and exerts essentially excitatory effects upon target neurons. The main function of histaminergic neurons is to trigger and maintain wakefulness and pro cognitive responses. Activation of histaminergic neurotransmission in brain is achieved via blockade of H3 receptors, and is currently explored as a treatment of wakefulness and cognitive deficits in several neurological and psychiatric diseases.

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Effects of GABA-Mimetic Drugs on Turnover of Histamine in the Mouse Brain

Cited by 10 publications

References 16 publications

Rapid changes in glutamate levels in the posterior hypothalamus across sleep-wake states in freely behaving rats

Rapid changes in glutamate levels in the posterior hypothalamus across sleep-wake states in freely behaving rats

Endogenous GABA Modulates Histamine Release from the Anterior Hypothalamus of the Rat

Neuropharmacology of Histamine in Brain

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