Dexfenfluramine action

Dexfenfluramine caused serotonin release and inhibited reuptake at moderately low concentrations. It also stimulated 5-HT receptors at relatively low concentrations. Metergoline, an ergot derivative with high affinity for 5-HT receptors, completely blocked the anorexiant effect of dexfenfluramine, further suggesting a serotonergic action. 

MR-visible fluorinated compounds that can be measured in the human brain comprise a large number of psychiatric medications including most of the serotonin-specific reuptake inhibitors (SSRIs) such as fluoxetine (Prozac ) [1, 28, 41], as well as pharmaceuticals with mechanisms of action outside the central nervous system such as dexfenfluramine (fen-phen, a serotoninergic anorectic drug) [1, 31]. A recent review [1] covers the impact of MR spectroscopy in psychiatry. 

Two halogenated amphetamines, fenfluramine and dexfenfluramine, have been used to reduce appetite these drugs were withdrawn from the U.S. market after reports of cardiac toxicity associated with their use. The mechanism of action of this class of drugs is controversial. A profound reduction in levels of 5-HT in the brain lasts for weeks and is accompanied by a loss of proteins (5-HT transporter and tryptophan hydroxylase) selectively localized in 5-HT neurons, suggesting that the halogenated amphetamines have a neurotoxic action, although neuroanatomical signs of neuronal death are not readily apparent. 

A. Amphetamine and related drugs activate the sympathetic nen/ous system via central nervous system (CNS) stimulation, peripheral release of catecholamines, inhibition of neuronal reuptake of catecholamines, and inhibition of monoamine oxidase. Fenfluramine and dexfenfluramine cause serotonin release and block neuronal serotonin uptake. The various drugs have different profiles of action resulting in different levels of CNS and peripheral stimulation. 

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