The effect of prostaglandin E1 on acetylcholine release from the cat brain.

Cerebral ventricular perfusion with prostaglandin E1 (PGE1, 1.4 X 10(-8) M) reduced the release of acetylcholine (ACh) into the ventriculo-cisternal perfusate of the unanaesthetized cat's brain. The samples of effluent were assayed on the isolated guinea-pig ileum. Neither a halving (1.07 X 10(-3) M) nor a threefold rise (6.45 X 10(-3) M) in the calcium concentration of the perfusate had any effect on the spontaneous release of the cholinergic transmitter. The action of PGE1 was counteracted by decreasing and potentiated by increasing the extracellular calcium concentration. Polyphloretin phosphate (PPP, 10(-4) g/ml) in itself did not significantly affect the ACh outflow. Preperfusion however, with this drug readily antagonized the depressant effect of PGE1. Ouabain (2.0 X 10(-5) M) added to the perfusion fluid increased the ACh output from the cat brain, and PGE1 prevented this effect of ouabain. A single intraventricular injection of 6-hydroxydopamine (1 mg) counteracted the inhibitory effect of PGE1 on spontaneous ACh release. A perfusion with the potent PG synthesis inhibitor suprofen (3.8 X 10(-7) M) did not influence change the mean output of the transmitter. Our data indicate that PGE1 reduces ACh release in the CNS via a pre- or postsynaptic modification of monoaminergic neurotransmission.