Selective inhibitors of biosynthesis of aminergic neurotransmitters

Kollonitsch, J.; Patchett, Arthur A.; Marburg, Stephen; Maycock, Alan L.; Perkins, L.M.; Doldouras, G. A.; Duggan, D E; Aster, S.

doi:10.1038/274906a0

Cited by 434 publications

(196 citation statements)

References 20 publications

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“…ACh release was increased through the release of histamine, since both ACh and histamine electrically-evoked releases were abolished in rats pretreated with a-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase. This enzyme is essential for histamine synthesis [71], and its blockade caused a complete depletion of neuronal histamine [132]. ACh electrically-elicited release was inhibited by systemic administration of zolantidine, an H 2 receptor antagonist [21], but not of pyrilamine, an H 1 receptor antagonist, thus indicating that activation of H 2 receptors resulted in an increase of extracellular level of hippocampal ACh [83].…”

Section: Modulation Of Hippocampal Cholinergic Tone By Histaminementioning

confidence: 99%

Interactions between histaminergic and cholinergic systems in learning and memory

Bacciottini

Passani

Mannaioni

et al. 2001

Behavioural Brain Research

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The aim of this review is to survey biochemical, electrophysiological and behavioral evidence of the interactions between the cholinergic and histaminergic systems and evaluate their possible involvement in cognitive processes. The cholinergic system has long been implicated in cognition, and there is a plethora of data showing that cholinergic deficits parallel cognitive impairments in animal models and those accompanying neurodegenerative diseases or normal aging in humans. Several other neurotransmitters, though, are clearly implicated in cognitive processes and interact with the cholinergic system. The neuromodulatory effect that histamine exerts on acetylcholine release is complex and multifarious. There is clear evidence indicating that histamine controls the release of central acetylcholine (ACh) locally in the cortex and amygdala, and activating cholinergic neurones in the nucleus basalis magnocellularis (NBM) and the medial septal area-diagonal band that project to the cortex and to the hippocampus, respectively. Extensive experimental evidence supports the involvement of histamine in learning and memory and the procognitive effects of H 3 receptor antagonists. However, any attempt to strictly correlate cholinergic/histaminergic interactions with behavioral outcomes without taking into account the contribution of other neurotransmitter systems is illegitimate. Our understanding of the role of histamine in learning and memory is still at its dawn, but progresses are being made to the point of suggesting potential treatment strategies that may produce beneficial effects on neurodegenerative disorders associated with impaired cholinergic function.

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Section: Modulation Of Hippocampal Cholinergic Tone By Histaminementioning

confidence: 99%

Interactions between histaminergic and cholinergic systems in learning and memory

Bacciottini

Passani

Mannaioni

et al. 2001

Behavioural Brain Research

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“…The opioid-induced increase in BBB permeability to sodium fluorescein is inhib ited by an intracerebroventricular injection of H 2 -antagonists or a-fluoromethylhistidine (a-FMH) (Oishi et a!. , 1989a), a specific inhibitor of histidine decarboxylase (Kollonitsch et a!., 1978). Therefore, it is possible that brain HA is responsible for some of the pathological changes induced by brain isch emia.…”

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confidence: 99%

Direct Evidence for Increased Continuous Histamine Release in the Striatum of Conscious Freely Moving Rats Produced by Middle Cerebral Artery Occlusion

Adachi

Itoh

Oishi

et al. 1992

J Cereb Blood Flow Metab

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Summary: Extracellular histamine in the striatum of con scious freely moving rats collected by intracerebral mi crodialysis 1 day after implantation of a V-shaped dialysis probe was measured by HPLC coupled with postcolumn o-phthalaldehyde derivatization fluorometry. The basal fractional histamine outputs were almost constant from 1 to 7 h after the start of perfusion (5.9-8.4 pg/30 min). Depolarization by perfusion with a high K + (100 mM) containing medium produced a significant (124%) in crease and neuronal blockade by perfusion with a tetro dotoxin (1 jLM)-containing medium resulted in a 68% re duction in the histamine output. The histamine output was markedly reduced by intraperitoneal injection of o:-fluoromethylhistidine (100 mg/kg) , an irreversible in hibitor of histidine decarboxylase, or (R)-o:-methyl histamine (5 mg/kg), a potent and specific H3-receptor Histamine (HA) exists in at least two classes of cellular stores in the mammalian brain, i. e., neurons and mast cells (Schwartz et a!. , 1986). Histaminer gic fibers are widely distributed in the brain, origi nating from cell bodies in the posterior hypothala mus (Watanabe et a!. , 1984), and histaminergic in nervation of the cerebral microvasculature has also been demonstrated (Steinbusch and Verhofstad, 1986;Takagi et a!. , 1986).There is some evidence that brain HA may play an important role in the regulation of blood-brain barrier (BBB) permeability: carotid artery infusion of HA increases BBB permeability (Dux and J06, Received March 20, 1991; final revision received October I, 1991; accepted October 7, 1991. Address correspondence and reprint requests to Dr. K. Saeki at Department of Pharmacology, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama 700, Japan.Abbreviations used: BBB, blood-brain barrier; a-FMH, a-flu oromethylhistidine; HA, histamine; MeA, middle cerebral ar tery. (R)-a-MH, (R)-a-methylhistamine. 477agonist. After middle cerebral artery (MCA) occlusion, the histamine output gradually increased, and reached four times the control value 8 h later. When rats were pretreated with metoprine (10 mg/kg), a histamine N methyltransferase inhibitor, there was no significant dif ference in the histamine output between the MCA occluded and the sham-operated groups during the first 3.5 h after the operation, but the histamine output grad ually increased thereafter in the MCA-occluded group. In rats treated with o:-fluoromethylhistidine, MCA occlusion failed to cause an increase in the histamine output. These results demonstrate that MCA occlusion induces a long lasting increase in neuronal histamine release in the rat striatum.

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“…a-FMH is an irreversible and specific inhibitor of histidine decarboxylase [14,15] and even a single administration can deplete neuronal histamine in the animal brain [36,37]. Thus, a-FMH has been considered a useful tool to examine the functions of neuronal histamine in the brain.…”

Section: Discussionmentioning

confidence: 99%

“…The aim of the present study, thus, was to clarify the possible role of endogenous histamine on the rat cerebral somatostatinergic system. Therefore, we examined the effects of inhibition of histamine synthesis by the histidine decarboxylase inhibitor a-fluoromethylhistidine (a-FMH) [14,15] on SS receptors in rat frontoparietal cortex membranes. Since the post-receptor mechanism of action of SS includes, at least in part, the inhibition of adenylyl cyclase (AC) activity via GTP binding 'G proteins' [16,17], we have studied SS-inhibited AC activity in frontoparietal cortex membranes from control and a-FMH-treated rats.…”

Section: Introductionmentioning

confidence: 99%

α-Fluoromethylhistidine influences somatostatin content, binding and inhibition of adenylyl cyclase activity in the rat frontoparietal cortex

Puebla

Arilla

1995

Regulatory Peptides

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Selective inhibitors of biosynthesis of aminergic neurotransmitters

Cited by 434 publications

References 20 publications

Interactions between histaminergic and cholinergic systems in learning and memory

Interactions between histaminergic and cholinergic systems in learning and memory

Direct Evidence for Increased Continuous Histamine Release in the Striatum of Conscious Freely Moving Rats Produced by Middle Cerebral Artery Occlusion

α-Fluoromethylhistidine influences somatostatin content, binding and inhibition of adenylyl cyclase activity in the rat frontoparietal cortex

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