The evidence for the involvement of the 5-HT1A receptor in 5-HT syndrome induced in mice by tryptamine.

Yamada, Jun; Sugimoto, Yukihiko; Horisaka, Kazuyoshi

doi:10.1254/jjp.51.421

Cited by 12 publications

(2 citation statements)

References 11 publications

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“…39 Fenfluramine is well known to elicit a behavioral syndrome in rats and mice, characterized by tremor, rigidity, Straub tail (tail held upwards and erect), hindlimb abduction, lateral head weaving and reciprocal forepaw treading. 17,42,51 Dose-related induction of this syndrome with fenfluramine has been used as a measure of neuronal activation of the central serotonergic system. We reasoned that a dose of fenfluramine sufficient to elicit a behavioral change in mice would likely be associated with changes in cortical activity patterns.…”

Section: Fenfluramine Dosementioning

confidence: 99%

Regional cerebral cortical activation in monoamine oxidase A-deficient mice: differential effects of chronic versus acute elevations in serotonin and norepinephrine

Holschneider

Scremin

Huynh³

et al. 2000

Neuroscience

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Mice deficient in monoamine oxidase A have previously been shown to demonstrate a chronic elevation of serotonin and norepinephrine in the brain. Using the autoradiographic [14C]iodo-antipyrine method, we examined cerebral cortical blood flow in conscious, restrained four- to five-month-old knock-out and wild-type animals following the intraperitoneal administration of either saline or D-fenfluramine. Knock-out animals administered saline, compared to their wild-type counterparts, demonstrated a significantly higher regional cortical blood flow in somatosensory and barrel field neocortex, an area which previous histological studies have shown to be characterized by abnormal serotonergic projection fibers and absent barrel formation. Regional cortical blood flow was significantly lower in knock-out than in wild-type mice in the entorhinal and midline motor cortex, with non-significant decreases noted in the olfactory, piriform and retrosplenial cortices and the amygdala. We compared the above findings to those obtained in response to D-fenfluramine which, in conjunction with its metabolite D-norfenfluramine, results in acute elevations of brain levels of serotonin and norepinephrine. Administration of D-fenfluramine (21. 2mg/kg) resulted in changes in regional cortical perfusion in most brain regions of both knock-out and wild-type mice that were opposite to the genotypic differences seen in perfusion in response to saline. Fenfluramine significantly increased regional cortical blood flow in the allocortex (olfactory, piriform, entorhinal) and the amygdala, and significantly decreased regional cortical blood flow in the somatosensory, barrel field, midline motor and retrosplenial cortices. Changes in regional perfusion in response to fenfluramine were topographically equivalent in knock-out and wild-type mice, although in knock-out mice such changes were of greater magnitude. Our study suggests that the effects on regional cortical blood flow of a lifelong absence of monoamine oxidase A, and the consequent chronic increase in serotonin and norepinephrine, differ from those attributable to acute increases in these neurotransmitters following fenfluramine administration. Such a differential response may reflect neurodevelopmental abnormalities and/or effects of a chronic physiological adaptation on the regulation of cortical activation.

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Section: Fenfluramine Dosementioning

confidence: 99%

Regional cerebral cortical activation in monoamine oxidase A-deficient mice: differential effects of chronic versus acute elevations in serotonin and norepinephrine

Holschneider

Scremin

Huynh³

et al. 2000

Neuroscience

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“…The 5-HT1A receptors seem to contribute to symptoms such as myoclonus, hyperreflexia, vasomotor tone alterations, anxiety, increased respiratory rate, and hyperactivity [ 1 , 39 ]. This receptor has been associated with several behaviors consistent with SS in rats and mice, such as Straub's tail, walking backward, stepping with forepaws, head shaking, tremors, and hindlimb abduction [ 42 ]. Accordingly, these behaviors are more apparent in mice overexpressing 5-HT1A receptors [ 43 ].…”

Section: Reviewmentioning

confidence: 99%

Serotonin Syndrome: The Role of Pharmacology in Understanding Its Occurrence

Poian,

Chiavegatto

2023

Cureus

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Serotonin syndrome (SS) is a potentially fatal adverse drug reaction characterized by an exaggerated increase in serotonergic activity in the central and peripheral nervous systems. It presents a constellation of signs and symptoms related to behavioral changes, neuromuscular excitability, and autonomic instability. These symptoms can occur in both mild and severe forms. SS can be triggered by the therapeutic use of a drug that increases serotonin (5-HT) availability in the synaptic cleft or by the co-administration of two or more drugs that provide this increase. With the escalating use of antidepressants by the world's population, this adverse reaction may be more recurrent. However, SS is often overlooked by patients or not diagnosed by doctors. This review aims to improve awareness about SS and provide a pharmacological perspective to explain its occurrence. Evidence shows that other neurotransmitters may also be involved with the pathology of SS. Furthermore, SS and neuroleptic malignant syndrome (NMS) seem to be part of the same pathological spectrum, especially in atypical NMS cases. The emergence of the syndrome's symptoms may be closely related to pharmacokinetic and/or pharmacodynamic polymorphisms that lead to an increase in the 5-HT available to or 5-HT signaling by specific receptors, thus constituting an important area for future investigations.

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Effects of tryptamine on plasma glucagon levels in mice

et al. 1994

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Our previous study indicated that tryptamine induces a dose-related increase in plasma glucagon levels of mice and that this effect is mediated by the peripheral serotonin2 (5-HT2) receptor. The present paper further investigated the involvement of serotonergic and catecholaminergic systems in hyperglucagonemia elicited by tryptamine. An inhibitor of 5-HT synthesis, p-chlorophenylalanine, did not affect tryptamine-induced increases in plasma glucagon levels. Tryptamine-induced hyperglucagonemia was not inhibited by adrenalectomy or by an inhibition of catecholamine synthesis by alpha-methyl-p-tyrosine. These findings indicate that tryptamine-induced hyperglucagonemia is elicited by its direct activation of 5-HT2 receptors and is not mediated by levels of endogenous 5-HT and catecholamines. The results further suggest that the peripheral 5-HT2 receptor has a possible role in the release of glucagon.

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The evidence for the involvement of the 5-HT1A receptor in 5-HT syndrome induced in mice by tryptamine.

Cited by 12 publications

References 11 publications

Regional cerebral cortical activation in monoamine oxidase A-deficient mice: differential effects of chronic versus acute elevations in serotonin and norepinephrine

Regional cerebral cortical activation in monoamine oxidase A-deficient mice: differential effects of chronic versus acute elevations in serotonin and norepinephrine

Serotonin Syndrome: The Role of Pharmacology in Understanding Its Occurrence

Effects of tryptamine on plasma glucagon levels in mice

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