Correlation of prostaglandin release from the cerebral cortex of cats with the electrocorticogram, following stimulation of the reticular formation

Abstract

. Prostaglandin‐like material has been found in superfusates of cerebral cortex in unanaesthetized encéphale isolé cat preparations. . The material was assayed on the isolated rat uterus and identified by thin‐layer chromatography. . The level of spontaneous release of prostaglandin‐like material was greater than that which had been found in anaesthetized preparations and it increased further with electrical stimulation of the reticular formation which induced electrocortical arousal. . Chlorpromazine (1.0–8.0 mg/kg) not only depressed the spontaneous release but blocked the increase evoked by stimulation concomitantly with blocking electrocortical arousal. Increasing the stimulating voltage to restore the arousal response also restored the evoked release of prostaglandins. . Most of the prostaglandin‐like material released spontaneously was represented by E type compounds, but the increase with stimulation was mainly of F compounds.

Anorectic Activity of Prostaglandin Precursors

“…For example, gold thioglucose (Brecher & Waxler, 1949) and bipiperidyl mustard (Rutman, Lewis & Bloomer, 1966) have been shown to cause hyperphagia resulting in obesity in experimental animals, an effect which can be antagonized by prior treatment with indomethacin (Caffyn, 1972). In addition, a wide variety of clinically used drugs, for example psychotropics (Bainbridge, 1968), local anaesthetics (Epstein, 1960), A8-tetrahydrocannabinol (Rating, Broerman, Honecker, Kluwe & Coper, 1972) have been shown to increase food intake; although they are chemically diverse, all inhibit prostaglandin biosynthesis in vitro (Bradley, Samuels & Shaw, 1969;Burstein & Raz, 1972;Kunze, Bohn, Kurz & Vogt, 1973;Kunze, Bohn & Bahrke, 1975). Similarly, the anorectic activity of oleic acid (Booth, 1972) and methylxanthines (Fajardo, 1974) can possibly be explained by their in vitro inhibitory action on prostaglandin dehydrogenase (Flower, 1974).…”

Prostaglandin E1 causes sedation and increases 5‐hydroxytryptamine turnover in rat brain

“…They may be released into superfusates of the brain either spontaneously or by electrical stimulation (Coceani & Wolfe, 1965;Ramwell & Shaw, 1967;Bradley, Samuels & Shaw, 1969). It has been proposed that prostaglandins may be neurotransmitters or may modulate the activity of other neurohormones (Avanzino, Bradley & Wolstencroft, 1966a, b;Horton & Main, 1967a;Bradley et al, 1969).…”

Prostaglandin Inhibition and Cerebrovascular Control in Patients with Headache

“…25,26 Stimulation of the ascending reticular formation enhances cerebral PG synthesis. 27 Thus, PG synthesis is increased during arousal and decreased during drowsiness.…”