Neuronal and vascular localization of histamine N‐methyltransferase in the bovine central nervous system

Nishibori, Masahiro; Tahara, Akihito; Sawada, Ken; Sakiyama, Junko; Nakaya, Naoki; Saeki, Kiyomi

doi:10.1046/j.1460-9568.2000.00914.x

Cited by 36 publications

(21 citation statements)

References 44 publications

(94 reference statements)

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“…It has been demonstrated that HMT distribution in brain is not homogeneous (Bischoff and Korf, 1978;Nishibori et al, 2000) and thus, the effect of reserpine on HA catabolism in hypothalamus and cortex of rats might depend on the distribution and activity of HMT.…”

Section: Discussionmentioning

confidence: 99%

The metabolism of histamine in rat hypothalamus and cortex after reserpine treatment

Maldonado

Maeyama

2015

Neurochemistry International

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Section: Discussionmentioning

confidence: 99%

The metabolism of histamine in rat hypothalamus and cortex after reserpine treatment

Maldonado

Maeyama

2015

Neurochemistry International

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“…Histaminergic innervation of the HMN has been demonstrated in the rat (Panula et al, 1989) and guinea pig (Bouthenet et al, 1988). The HMN has also been shown to contain high amounts of HA Nmethyltransferase (Nishibori et al, 2000), which plays a crucial role in HA inactivation. HA neurons display wakingspecific discharge, becoming completely silent at sleep onset (Sakai et al, 1990;Takahashi et al, 2006;Vanni-Mercier et al, 2003).…”

Section: Ha and Gg Muscle Activitymentioning

confidence: 99%

Application of histamine or serotonin to the hypoglossal nucleus increases genioglossus muscle activity across the wake–sleep cycle

Neuzeret

Sakai

Gormand

et al. 2009

Journal of Sleep Research

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SUMMAR Y The decrease in genioglossus (GG) muscle activity during sleep, especially rapid eye movement (REM) or paradoxical sleep, can lead to airway occlusion and obstructive sleep apnoea (OSA). The hypoglossal nucleus innervating the GG muscle is under the control of serotonergic, noradrenergic and histaminergic neurons that cease firing during paradoxical sleep. The objectives of this study were to determine the effect on GG muscle activity during different wake-sleep states of the microdialysis application of serotonin, histamine (HA) or noradrenaline (NE) to the hypoglossal nucleus in freely moving cats. Six adult cats were implanted with electroencephalogram, electrooculogram and neck electromyogram electrodes to record wake-sleep states and with GG muscle and diaphragm electrodes to record respiratory muscle activity. Microdialysis probes were inserted into the hypoglossal nucleus for monoamine application. Changes in GG muscle activity were assessed by power spectrum analysis. In the baseline conditions, tonic GG muscle activity decreased progressively and significantly from wakefulness to slow-wave sleep and even further during slow-wave sleep with ponto-geniculo-occipital waves and paradoxical sleep. Application of serotonin or HA significantly increased GG muscle activity during the wake-sleep states when compared with controls. By contrast, NE had no excitatory effect. Our results indicate that both serotonin and HA have a potent excitatory action on GG muscle activity, suggesting multiple aminergic control of upper airway muscle activity during the wake-sleep cycle. These data might help in the development of pharmacological approaches for the treatment of OSA.k e y w o r d s genioglossus, histamine, hypoglossus, noradrenaline, obstructive sleep apnoea, serotonin, sleep INTRODUCTIONThe activity of the genioglossus (GG) muscle, innervated by the hypoglossal (XII) motor nucleus (HMN), contributes to the maintenance of upper airway patency (Ryan and Bradley, 2005;White, 2006). During sleep, especially rapid eye movement (REM) or paradoxical sleep (PS), GG muscle activity decreases in animals (Horner et al., 2002;Megirian et al., 1985) and humans (Katz and White, 2004;Sauerland and Harper, 1976). In individuals with an anatomically small pharyngeal airway, this decrease in GG muscle activity can lead to airway occlusion (Remmers et al., 1978), i.e. obstructive sleep apnoea (OSA), a sleep disorder affecting up to 4% of adults (Young et al., 1993). The mechanisms responsible for this selective obstruction of the upper airway during PS remain unclear and pharmacological therapies have not Correspondence: Pierre-Charles Neuzeret, INSERM U628, Physiologie Inte´gre´e du Syste`me dÕEveil,

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“…Stored histamine in specialized secretory vesicles is released by depolarization stimuli both in vivo and in vitro [20,21,23,36,40] . Inactivation of released histamine is believed to proceed by its direct enzymatic transformation to N -methylimidazole acetic acid through N -tele-methylation by histamine N -tele-methyltransferase (EC 2.1.1.8) and oxidative deamination by monoamine oxidase B (EC 1.4.3.4) and aldehyde dehydrogenase (EC 1.2.1.3) [7,16,26,42] . Histamine is transported into both neuronal and glial cells, and inactivated in these cells [16] .…”

mentioning

confidence: 99%

“…Inactivation of released histamine is believed to proceed by its direct enzymatic transformation to N -methylimidazole acetic acid through N -tele-methylation by histamine N -tele-methyltransferase (EC 2.1.1.8) and oxidative deamination by monoamine oxidase B (EC 1.4.3.4) and aldehyde dehydrogenase (EC 1.2.1.3) [7,16,26,42] . Histamine is transported into both neuronal and glial cells, and inactivated in these cells [16] . However, the transport system of neuronal histamine is still unclear, although there was a paper on uptake of [ 14 C]histamine into rat synaptosomes [43] .…”

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confidence: 99%

Evidence for the Presence of Histamine Uptake into the Synaptosomes of Rat Brain

Sakurai

Oreland

et al. 2006

Pharmacology

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Histamine has many physiological roles in the brain and periphery. Neuronal histamine is metabolized almost exclusively by histamine N-methyltransferase. Although several neurotransmitter systems such as dopamine and 5-hydroxytryptamine have their specific reuptake system in their neurons and glial cells, a specific histamine reuptake system into the corresponding nerve terminals or glial cells has not yet been clearly elucidated. We characterized the uptake of histamine into the P2 fractions of rat brain homogenized in 0.32 mol/l sucrose using in vitro uptake techniques. [³H]histamine uptake increased with the increment of added protein amount and elapsed time. [³H]histamine uptake was also temperature-dependent. The uptake of [³H]histamine into the P2 fractions occurs by two saturable processes, a high-affinity and a low-affinity, characterized by K_m values of 0.16 and 1.2 µmol/l, respectively. Na⁺, Cl^– and HCO₃^– ions were essential for the uptake of histamine in P2 fractions. [³H]histamine uptake was inhibited in the presence of several tricyclic antidepressants. In accordance with this, the endogenous release of histamine from brain slices evoked by 100 mmol/l K⁺ was augmented in the presence of 20 µmol/l imipramine. These results further support the existence of a specific histamine uptake system in the brain, although the precise molecular entities have not been identified until now.

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Neuronal and vascular localization of histamine N‐methyltransferase in the bovine central nervous system

Cited by 36 publications

References 44 publications

The metabolism of histamine in rat hypothalamus and cortex after reserpine treatment

The metabolism of histamine in rat hypothalamus and cortex after reserpine treatment

Application of histamine or serotonin to the hypoglossal nucleus increases genioglossus muscle activity across the wake–sleep cycle

Evidence for the Presence of Histamine Uptake into the Synaptosomes of Rat Brain

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