Structure and Functions of the Histaminergic Neurone System

Yamatodani, Atsushi; Inagaki, Naoyuki; Panula, Pertti; Itowi, Nobuko; Watanabe, Takehiko; Wada, Hiroshi

doi:10.1007/978-3-642-75840-9_16

Cited by 41 publications

(22 citation statements)

References 317 publications

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“…37 Histaminergic neurons play an important role in the regulation of energy balance and feeding via the activation of postsynaptic histamine H 1 receptors. 9,21,22 In male rats, food intake is inversely correlated with the density of brain histamine H 1 receptors. 38 Portacaval surgery results in a significant weight loss immediately after the procedure.…”

Section: Discussionmentioning

confidence: 99%

“…Histaminergic signaling is mediated by 3 types of receptors, histamine H 1 , H 2 , and H 3 receptors, distinguished by their pharmacologic properties, specific anatomic location, and by the intracellular responses they mediate. 11,12 Interest has focused on the histamine H 1 receptors, because histamine, through the activation of the postsynaptic histamine H 1 receptors, is involved in the regulation of the neuroendocrine system, 13,14 locomotor activity, 15-17 circadian rhythmicity, 18,19 and the sleep-wake cycle, 20 as well as in various behaviors, including feeding and drinking (for a review, see Schwartz, 9 Yamatodani et al, 21 and Sakata 22 ).We have previously shown that altered histaminergic neurotransmission is an important part of the neurophysiologic background responsible for the behavioral changes after PCA surgery in the rat, leading us to propose that it may contribute to the pathogenesis of HE in human subjects. [6][7][8] Relating the functions controlled by histamine to the clinical presentation of HE, it appears a priori that histamine could participate in the pathogenesis of the sleep disturbances, decreased spontaneous voluntary movement, and increased plasma prolactin levels in patients with HE and in the hormonal changes, growth retardation, and the altered vigilance, locomotor activity, and circadian rhythmicity in rats with PCA.…”

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Increased density of brain histamine H1 receptors in rats with portacaval anastomosis and in cirrhotic patients with chronic hepatic encephalopathy

Lozeva¹

2001

Hepatology

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The binding properties and the regional densities of histamine H 1 receptors were studied in brain of rats with portacaval anastomosis (PCA) and in autopsied brain tissue from cirrhotic patients with hepatic encephalopathy (HE). Receptor binding studies and quantitative receptor autoradiography were performed, employing [ 3 H]mepyramine. Histamine H 1 receptors in rat brain displayed a higher density and a lower affinity compared with control human frontal cortex. Specific [ 3 H]mepyramine binding was heterogeneously distributed throughout the brain in both species. In human brain, binding was highest in the parietal and temporal cortices and lowest in caudate-putamen. In rat brain, binding was highest in the suprachiasmatic nucleus, dentate gyrus of the hippocampus, ventromedial hypothalamus, and nucleus accumbens. Hepatic encephalopathy (HE) is a potential long-term complication of chronic liver disease. Despite extensive research and a succession of different hypotheses, the exact mechanisms underlying the development of the clinical symptoms of HE are not well understood. 1,2 Consequently, progress in the treatment of HE in cirrhotic patients has been limited. Among the least exploited consequences of HE are the marked changes in the brain histaminergic system, which have been previously documented both in patients with HE 3 and in rats with portacaval anastomosis (PCA), a well-established animal model of the disease. [4][5][6][7][8] There is substantial evidence that histamine acts as a neurotransmitter in mammalian brain. 9 Histaminergic neurons are located exclusively in the tuberomammillary nucleus of the posterior hypothalamus and send their varicose fibers to almost every region of the brain. 10 This widespread distribution of histaminergic neurons suggests that the brain histaminergic system is involved in the regulation of a wide range of neurobiologic functions. Histaminergic signaling is mediated by 3 types of receptors, histamine H 1 , H 2 , and H 3 receptors, distinguished by their pharmacologic properties, specific anatomic location, and by the intracellular responses they mediate. 11,12 Interest has focused on the histamine H 1 receptors, because histamine, through the activation of the postsynaptic histamine H 1 receptors, is involved in the regulation of the neuroendocrine system, 13,14 locomotor activity, 15-17 circadian rhythmicity, 18,19 and the sleep-wake cycle, 20 as well as in various behaviors, including feeding and drinking (for a review, see Schwartz, 9 Yamatodani et al., 21 and Sakata 22 ).We have previously shown that altered histaminergic neurotransmission is an important part of the neurophysiologic background responsible for the behavioral changes after PCA surgery in the rat, leading us to propose that it may contribute to the pathogenesis of HE in human subjects. [6][7][8] Relating the functions controlled by histamine to the clinical presentation of HE, it appears a priori that histamine could participate in the pathogenesis of the sleep disturbances, decreased spontaneous vo...

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Section: Discussionmentioning

confidence: 99%

mentioning

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confidence: 99%

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Increased density of brain histamine H1 receptors in rats with portacaval anastomosis and in cirrhotic patients with chronic hepatic encephalopathy

Lozeva¹

2001

Hepatology

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“…Recently, type-2 astrocytes have been shown to express glutamate receptors (11,12), suggesting that they are also involved in cell-to-cell communication in the central nervous system. Histamine acts as one of the signal messengers released from neurons (13)(14)(15), and previous studies have shown that mixed cultures of type-2 and type-1 astrocytes express histamine H1 receptors (16, 17), activation of which produces Ins(1,4,5)P3 (14). In the present study, we examined the effects of histamine on [Ca2+], of type-2 astrocytes by fura-2-based digital imaging fluorescence microscopy (4,5 (18,19), as reported previously (20).…”

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Single type-2 astrocytes show multiple independent sites of Ca2+ signaling in response to histamine.

Inagaki

Fukui

Ito

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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MATERIALS AND METHODSPreparation of Cell Cultures. Primary cultures of type-2 astrocytes were prepared from the cerebrum, where dense histaminergic fibers distribute in the brain (18,19), as reported previously (20). Newborn Wistar rats were killed by decapitation. The cerebral hemispheres were collected in Joklik's modified minimum essential medium (MEM) under sterile conditions and the meninges were carefully removed using an operation microscope. The cerebral hemispheres were triturated mechanically with a pipette and then dissociated enzymatically with dispase (neutral protease, dispase grade II) solution (3 mg/ml) in Joklik's modified MEM as reported (17). The dissociated cells in the culture medium (Eagle's MEM containing 10% fetal calf serum, 100.units of penicillin G per ml, and 60 ,ug of kanamycin per ml) were seeded in culture flasks (75 cm2) at a density of 1 x i0' cells per cm2. The cultures were incubated at 37°C in a humid atmosphere of95% air/5% C02; the medium was changed the next day and twice a week thereafter. After 2 weeks in vitro, the small process-bearing 0-2A progenitor cells (21) grown on the top of the type-i astrocyte monolayer were removed mechanically by shaking the culture flasks overnight, seeded onto glass coverslips attached to silicon walls (Heraeus Flexiperm Disc), and subcultured in the same medium containing fetal calf serum for differentiation into type-2 astrocytes (21, 22). After 7 days, >70% of the cultured cells exhibited the characteristics of type-2 astrocytes-i.e., they were stellate cells immunoreactive to antiglial fibrillary acid protein (GFAP) and A2B5 (23) 4215The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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“…These neuronal groups are named as E1-E5 groups [5,6,7], by analogy with other monoaminergic neuron systems: noradrenergic, Al-A7; dopaminergic, A8-A17; serotoninergic, B1-B9; adrenergic, C1-C3 (Fig.1). The El and E2 groups are located in the lateral surface of the mammillary body, and caudally situated E1 group is separated from the rostral E2 group by the lateral mammillary nucleus.…”

Section: Cell Bodies Of the Histaminergic Neuronsmentioning

confidence: 99%