Abstract

Several recent studies indicate that the symptoms of the premenstmal syndrome (PMS) are associated with an attenuation of peripheral serotonergic mechanisms, such as decreased platelet 5-hydroxytryptamine (5-HT) uptake and content (Ashby et al 1988; Taylor et al 1984), as well as changes in whole blood 5-HT levels (Rapkin et al 1987). As numerous biochemical and pharmacological studies have indicated that the platelet may be a model for central serotonergic neurons (Stahl 1985), it is possible that serotonergic neuronal function in the brain may be altered during the symptomatic phase of PMS. Angel and Paul (1984) and Brusov et al (1985) have demonstrated that plasma and plasma extracts from humans and rats contain endogenous substances that appear to selectively inhibit 5HT uptake in blood platelets, as well as rat brain synaptosomes. Thus, some of the symptoms of PMS could result from the presence of endogenous factors which alter brain 5-HT uptake. A

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