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

1

Administration of prostaglandin E₁ (1 mg/kg, i.p.) to rats induced sedation and a decrease in muscular tone. Prostaglandin E₁‐induced sedation was accompanied by the low voltage—high frequency E.E.G. pattern characteristic of the waking animal.

Administration of prostaglandin E₁ (1 mg/kg, i.p.) to rats induced sedation and a decrease in muscular tone. Prostaglandin E₁‐induced sedation was accompanied by the low voltage—high frequency E.E.G. pattern characteristic of the waking animal.

Administration of prostaglandin E₁ also increased the turnover rate of 5‐hydroxytryptamine and raised the concentration of acetylcholine in brain.

The behavioural effects of prostaglandin were blocked by prior administration of p‐chlorophenylalanine or pargyline, drugs which lowered the brain concentration of 5‐hydroxyindoleacetic acid (5‐HIAA), and was potentiated by pretreatment with probenecid, which elevated the 5‐HIAA concentration. Pretreatment with atropine sulphate failed to alter prostaglandin E₁‐induced sedation.

The results are compatible with the possibility that prostaglandin E₁ induces a state resembling paradoxical sleep through an action on 5‐hydroxytryptamine metabolism in brain.

DOI: 10.1111/j.1476-5381.1973.tb08224.x

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