Monoaminergic neurons, chemosensation and arousal

Haxhiu, Musa A.; Tolentino‐Silva, Fatima; Pete, Gina; Kc, Prabha; Mack, Serdia O.

doi:10.1016/s0034-5687(01)00290-0

Cited by 74 publications

(61 citation statements)

References 87 publications

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“…This view is challenged by the current study, which supports the idea that subsets of histaminergic neurons form independent functional units modulated by selective mechanisms according to their respective origin and terminal projections. Much evidence favoring this hypothesis has been reported recently, with findings demonstrating that histamine neurons differ in their sensitivity to glycine (Sergeeva et al, 2001), GABA (Sergeeva et al, 2005;Giannoni et al, 2009), types of stress (Miklos and Kovacs, 2003), bicuculline or thioperamide (Giannoni et al, 2009), and hypercapnic loading (Haxhiu et al, 2001). Although further studies are required to understand the full implications of such functional heterogeneity of histaminergic neurons, H 3 R antagonists may affect only some of those functions.…”

Section: Discussionmentioning

confidence: 97%

Regional Differential Effects of the Novel Histamine H₃ Receptor Antagonist 6-[(3-Cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254) on Histamine Release in the Central Nervous System of Freely Moving Rats

Giannoni¹,

Medhurst²,

Passani³

et al. 2009

J Pharmacol Exp Ther

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After oral administration, the nonimidazole histamine H 3 receptor antagonist, 6-[(3-cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254), increased histamine release from the tuberomammillary nucleus, where all histaminergic somata are localized, and from where their axons project to the entire brain. To further understand functional histaminergic circuitry in the brain, dual-probe microdialysis was used to pharmacologically block H 3 receptors in the tuberomammillary nucleus, and monitor histamine release in projection areas. Perfusion of the tuberomammillary nucleus with GSK189254 increased histamine release from the tuberomammillary nucleus, nucleus basalis magnocellularis, and cortex, but not from the striatum or nucleus accumbens. Cortical acetylcholine (ACh) release was also increased, but striatal dopamine release was not affected. When administered locally, GSK189254 increased histamine release from the nucleus basalis magnocellularis, but not from the striatum. Thus, defined by their sensitivity to GSK189254, histaminergic neurons establish distinct pathways according to their terminal projections, and can differentially modulate neurotransmitter release in a brain region-specific manner. Consistent with its effects on cortical ACh release, systemic administration of GSK189254 antagonized the amnesic effects of scopolamine in the rat object recognition test, a cognition paradigm with important cortical components. The discovery of the histamine H 3 receptor (H 3 R) back in 1983 was a major scientific breakthrough that provided key new perspectives in histamine research (Arrang et al., 1983). Originally detected on varicosities of histaminergic axons as an autoreceptor that restricts histamine synthesis and release (Arrang et al., 1987), the H 3 R is also located on histaminergic somata where it provides a tonic inhibition. Indeed, application of the H 3 R antagonist thioperamide enhanced the firing of histaminergic neurons (Haas and Panula, 2003). These neurons arise solely from the tuberomammillary nucleus (TMN) of the posterior hypothalamus, from where they send diffuse projections throughout the entire central nervous system (Inagaki et al., 1988;Panula et al., 1989). Consistent with this wideranging output, histamine is directly and indirectly involved in a variety of basic homeostatic and higher brain functions, such as the control of the sleep-wake cycle, appetite, nociception, cognition, and emotion (Haas and Panula, 2003;Passani et al., 2004), and H 3 R antagonists have been shown to increase wakefulness, improve cognitive performance, and reduce body weight in animal mod-

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Section: Discussionmentioning

confidence: 97%

Regional Differential Effects of the Novel Histamine H₃ Receptor Antagonist 6-[(3-Cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254) on Histamine Release in the Central Nervous System of Freely Moving Rats

Giannoni¹,

Medhurst²,

Passani³

et al. 2009

J Pharmacol Exp Ther

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“…Indeed, ascending drive from the caudal medulla appears to exert arousing or sedating actions depending upon the context. For example, "satiety" signals (e.g., cholecystokinin) known to activate hypothalamic noradrenergic input from the lower brainstem (Rinaman et al, 1995) do have a mildly sedating effect, whereas medullary catecholaminergic input of the hypothalamus related to hypercapnia may contribute to behavioral arousal (Haxhiu et al, 2001;Johnson et al, 2005), and those responsive to glucoprivic conditions induced by insulin or 2-deoxy glucose injections would generate feeding responses (Ritter et al, 2001). Thus, LPS challenge may activate a subtly different population of medullary catecholaminergic neurons than those associated with arousing stimuli such as hypercapnia or glucoprivation but may overlap with those driven by, e.g., satiety factors associated with sedation.…”

Section: Mechanisms Of Lps-induced Inhibition Of Histaminergic Neuronsmentioning

confidence: 99%

Lipopolysaccharide suppresses activation of the tuberomammillary histaminergic system concomitant with behavior: A novel target of immune-sensory pathways

et al. 2008

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Infection and inflammation strongly inhibit a variety of behaviors, including exploration, social interaction, and food intake. The mechanisms that underlie sickness behavior remain elusive, but appear to involve fatigue and a state of hypo-arousal. Because histaminergic neurons in the ventral tuberomammillary nucleus of the hypothalamus (VTM) play a crucial role in the mediation of alertness and behavioral arousal, we investigated whether the histaminergic system represents a target for immune activation and, if so, whether modulation by ascending medullary immune-sensitive projections represents a possible mechanism. Rats were injected intraperitoneally with either the proinflammatory stimulus lipopolysaccharide (LPS) or saline, exposed to one of various behavioral tests that would induce motivated behavior (exploration, play behavior, social interaction, sweetened milk consumption). Upon sacrifice, brains were processed for c-Fos and histidine decarboxylase immunoreactivity. LPS treatment reduced behavioral activity and blocked behavioral testassociated c-Fos induction in histaminergic neurons of the VTM. These effects of LPS were prevented by prior inactivation of the caudal medullary dorsal vagal complex (DVC) with a local anesthetic. To determine whether LPS-responsive brainstem projection neurons might provide a link from the DVC to the VTM, the tracer Fluorogold was iontophoresed into the VTM a week prior to experiment. Retrogradely labeled neurons that expressed c-Fos in response to LPS treatment included catecholaminergic neurons within the nucleus of the solitary tract and ventrolateral medulla. These findings support the hypothesis that the histaminergic system represents an important component in the neurocircuitry relevant for sickness behavior that is linked to ascending pathways originating in the lower brainstem. Keywordsarousal; sickness behavior; hypothalamus; dorsal vagal complex; dopamine-beta-hydroxylase; c-fos Converging lines of evidence strongly implicate histamine in the mammalian brain in behavioral arousal, wakefulness, metabolic homeostasis, and learning (Haas and Panula, 2003). The activity of the histaminergic neurons in the ventral tuberomammillary nucleus (VTM) is strongly and positively correlated with an alert waking state and behavioral activity,

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“…5-HT neurons respond to hypercapnic acidosis with an increase in activity in vitro (Richerson, 1995;Wang et al, 2001), and in vivo (Larnicol et al, 1994;Veasey et al, 1995;Haxhiu et al, 2001;Johnson et al, 2005), and this causes an increase in 5-HT release in vivo (Kanamaru and Homma, 2007), indicating that 5-HT neurons are modulated by the acid/base status of the brain. There is also evidence for a trophic role for 5-HT, especially during development and after CNS injury (Golder and Mitchell, 2005), as well as a permissive effect for some forms of plasticity such as long-term facilitation of respiratory motor output (Baker-Herman et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Defects in Breathing and Thermoregulation in Mice with Near-Complete Absence of Central Serotonin Neurons

Hodges¹,

Tattersall²,

Harris³

et al. 2008

J. Neurosci.

291

348

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f/f/p mice was decreased by 50% compared with wild-type mice, whereas baseline ventilation and the hypoxic ventilatory response were normal. In addition, Lmx1b f/f/p mice rapidly became hypothermic when exposed to an ambient temperature of 4°C, decreasing core temperature to 30°C within 120 min. This failure of thermoregulation was caused by impaired shivering and nonshivering thermogenesis, whereas thermosensory perception and heat conservation were normal. Finally, intracerebroventricular infusion of 5-HT stimulated baseline ventilation, and rescued the blunted hypercapnic ventilatory response. These data identify a previously unrecognized role of 5-HT neurons in the CO 2 chemoreflex, whereby they enhance the response of the rest of the respiratory network to CO 2 . We conclude that the proper function of the 5-HT system is particularly important under conditions of environmental stress and contributes significantly to the hypercapnic ventilatory response and thermoregulatory cold defense.

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Monoaminergic neurons, chemosensation and arousal

Cited by 74 publications

References 87 publications

Regional Differential Effects of the Novel Histamine H₃ Receptor Antagonist 6-[(3-Cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254) on Histamine Release in the Central Nervous System of Freely Moving Rats

Regional Differential Effects of the Novel Histamine H₃ Receptor Antagonist 6-[(3-Cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254) on Histamine Release in the Central Nervous System of Freely Moving Rats

Lipopolysaccharide suppresses activation of the tuberomammillary histaminergic system concomitant with behavior: A novel target of immune-sensory pathways

Defects in Breathing and Thermoregulation in Mice with Near-Complete Absence of Central Serotonin Neurons

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Monoaminergic neurons, chemosensation and arousal

Cited by 74 publications

References 87 publications

Regional Differential Effects of the Novel Histamine H3 Receptor Antagonist 6-[(3-Cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254) on Histamine Release in the Central Nervous System of Freely Moving Rats

Regional Differential Effects of the Novel Histamine H3 Receptor Antagonist 6-[(3-Cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254) on Histamine Release in the Central Nervous System of Freely Moving Rats

Lipopolysaccharide suppresses activation of the tuberomammillary histaminergic system concomitant with behavior: A novel target of immune-sensory pathways

Defects in Breathing and Thermoregulation in Mice with Near-Complete Absence of Central Serotonin Neurons

Contact Info

Product

Resources

About

Regional Differential Effects of the Novel Histamine H₃ Receptor Antagonist 6-[(3-Cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254) on Histamine Release in the Central Nervous System of Freely Moving Rats

Regional Differential Effects of the Novel Histamine H₃ Receptor Antagonist 6-[(3-Cyclobutyl-2,3,4,5-tetrahydro-1H-3-benzazepin-7-yl)oxy]-N-methyl-3-pyridinecarboxamide hydrochloride (GSK189254) on Histamine Release in the Central Nervous System of Freely Moving Rats