5‐HYDROXYTRYPTAMINE UPTAKE INHIBITORS BLOCK <i>para</i>‐METHOXYAMPHETAMINE‐INDUCED 5‐HT RELEASE

Tseng, Leon F.

doi:10.1111/j.1476-5381.1979.tb13663.x

Cited by 7 publications

(4 citation statements)

References 9 publications

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“…The range of agents examined encompasses the metabolic precursors of serotonin, L-tryptophan and L-5-hydroxytryptophan [1,3,6,10,17]; releasers such as fenfluramine [37], chloroamphetamine [ 12], and methoxyamphetamine [9]; uptake inhibitors (e.g., fluoxetine [17]), chlorimipramine [10]; and receptor agonists, such as 2,5-methoxyamphetamine [38], tryptamine [1], 5-methoxydimethyltryptamine [ 1,17], MK212 [ 1 ], and quipazine [1]. The latter two compounds are remarkable in that their effects show a dose-dependence over a 100-fold range, with peak swallowing rates (~ 100/min) approaching the maximum frequency obtainable with electrical stimulation of the superior laryngeal nerve.…”

Section: Serotoninergic Mechanismsmentioning

confidence: 99%

“…In predictable fashion, agents capable of releasing catecholamines from neuronal storage pools stimulate deglutition, as exemplified by (+)-amphetamine [3,6,12,26] and meta-methoxyamphetamine [9][10][11]. Catecholaminergic stimulation was initially attributed solely to an action at dopamine receptors [3], on account of the excitant action of the direct dopmine receptor agonist, apomorphine, and the lack of action of D,L-threo-3,4-dihydroxyphenylserine, which can undergo direct conversion to noradrenaline [30].…”

Section: Catecholaminergic Mechanismsmentioning

confidence: 99%

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Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

Bieger

1991

Dysphagia

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Pharmacologic investigations into the transmission processes underlying fictive swallowing in the rat have disclosed the potential diversity of chemical signals used in central deglutitive pathways. Monoaminergic mechanisms appear to serve as links between subcortical structures and the medullary pattern generator of swallowing (PGS), and may play a critical role in maintaining internal facilitatory drive, required by the PGS for optimal responsivity to peripheral sensory input. Cholinergic bulbar interneurons form an integral component of the PGS subnetwork controlling esophageal peristalsis. Local GABA neurons exert a tonic inhibition of the buccopharyngeal stage, may regulate buccopharyngeal-esophageal coupling, and may contribute to peristaltic rhythmic generation at both the premotoneuronal and motoneuronal level. Receptor subtypes for excitatory amino acids (glutamate, aspartate) are differentially associated with deglutitive premotoneurons for both the buccopharyngeal and esophageal stage, as well as with ambiguus motoneurons. Preliminary evidence suggests the existence of excitatory peptidergic mechanisms involving thyrotropin-releasing hormone, vasopressin, oxytocin, and somatostatin, a probable candidate for excitatory transmitter in the solitarioambigual internuncial projection to motoneurons innervating esophageal striated musculature. Further validation of this experimental model may ultimately help to establish a framework for the clinical recognition, management, and exploitation of drug actions on central deglutitive neuroeffectors.

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Section: Serotoninergic Mechanismsmentioning

confidence: 99%

Section: Catecholaminergic Mechanismsmentioning

confidence: 99%

Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

Bieger

1991

Dysphagia

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“…5 Early studies with PMA have revealed that PMA administration results in myoclonic twitch activity and induces release of 5-HT in the central nervous system. 6 It has also been demonstrated that PMA induces hyperthermia and that this hyperthermia is primarily a result of influence on the 5-HT system. 7 In vitro studies have revealed that PMA is more than 20 times as potent as (+)-amphetamine as an inhibitor of 5-HT oxidation by monoamine oxidase in mouse brain with a K I value of 0.22 µM.…”

Section: Introductionmentioning

confidence: 99%

“…Early studies with PMA have revealed that PMA administration results in myoclonic twitch activity and induces release of 5‐HT in the central nervous system 6. It has also been demonstrated that PMA induces hyperthermia and that this hyperthermia is primarily a result of influence on the 5‐HT system 7.…”

Section: Introductionmentioning

confidence: 99%

Comparative Effects of Substituted Amphetamines (PMA, MDMA, and METH) on Monoamines in Rat Caudate

Gough

Imam

Blough

et al. 2002

Annals of the New York Academy of Sciences

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Paramethoxyamphetamine (PMA) is a methoxylated phenethylamine derivative that has been used illicitly in Australia since 1994. PMA is also becoming popular at rave parties in the United States. PMA raised concern when a series of fatalities resulted after its use in South Australia, where it was marketed as “ecstasy,” which is the colloquial name for MDMA. In the present study, we evaluated the comparative neurotoxicity of substituted amphetamines in rats. Extracellular levels of dopamine (DA), 3,4‐dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5‐HT), and 5‐hydroxyindoleacetic acid (5‐HIAA) were assayed in the caudate of freely moving rats using microdialysis and HPLC‐EC. Dialysates were assayed every 20 minutes for 4 hours after an intraperitoneal (i.p.) injection of PMA (2.5, 5, 10, 20 mg/kg), MDMA (10 and 20 mg/kg), or METH (2.5 mg/kg). METH produced a significant increase in extracellular DA (700%), and significant decreases in extracellular DOPAC and HVA (30% and 50%), with no detectable changes in either 5‐HT or 5‐HIAA. MDMA produced significant increases in DA (700% at 10 mg/kg and 950% at 20 mg/kg) and decreases in DOPAC (15% for both 10 and 20 mg/kg), and HVA (50% at 10 mg/kg and 35% at 20 mg/kg). MDMA also increased 5‐HT (350% at 10, and 575% at 20 mg/kg), and decreased 5‐HIAA to 60% for both dose levels. PMA produced no detectable increases in DA at dose levels of 2.5, 5, or 10 mg/kg, but significantly increased DA (975%) at a dose of 20 mg/kg. However, PMA significantly decreased DOPAC at all dose levels (75% at 2.5; 40% at 5; 30% at 10; 10% at 20 mg/kg), with comparable decreases in HVA at all dose levels. PMA also produced significant increases in 5‐HT at 10 and 20 mg/kg (350% for both dose levels), with no detectable changes in 5‐HT at 2.5 or 5 mg/kg. All dose levels of PMA significantly decreased 5‐HIAA (50 to 70%). These data suggest that PMA, like MDMA and METH, is capable of producing dopaminergic and serotonergic neurotoxicity.

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The stimulus properties of para-methoxyamphetamine: A nonessential serotonergic component

Winter

1984

Pharmacology Biochemistry and Behavior

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5‐HYDROXYTRYPTAMINE UPTAKE INHIBITORS BLOCK para‐METHOXYAMPHETAMINE‐INDUCED 5‐HT RELEASE

Cited by 7 publications

References 9 publications

Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

Neuropharmacologic correlates of deglutition: Lessons from fictive swallowing

Comparative Effects of Substituted Amphetamines (PMA, MDMA, and METH) on Monoamines in Rat Caudate

The stimulus properties of para-methoxyamphetamine: A nonessential serotonergic component

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