Enhancement Of Acetylcholine Release Research Articles

Morphine enhancement of acetylcholine release from the brain in unanaesthetized cats

I.p. or i.v. administration of 5.0 and 0.5, but not 0.05, mg/kg of morphine to unanaesthetized cats caused a dose-related efflux of acetylcholine into the cerebral lateral ventricle and from the cerebral cortex. Pretreatment with naloxone, 0.1 mg/kg, prevented the morphine-induced increased release.

THE ACTION OF TRIETHYLCHOLINE ON THE PERISTALTIC REFLEX OF THE GUINEA-PIG ILEUM.

The action of triethylcholine on the peristaltic reflex of the guinea-pig isolated ileum has been studied. When perfused through the lumen in low concentrations triethylcholine first stimulated and then inhibited peristalsis. High concentrations gradually inhibited or abolished the reflex without prior stimulation. These inhibitory effects were reversed by choline, in the continued presence of triethylcholine. Similar responses followed application of triethylcholine to the serosal surface of the gut, except that high concentrations produced an immediate abolition of peristalsis which was not restored by choline. It is suggested that the effects of intraluminal triethylcholine are due either to enhancement of acetylcholine release or to reduction of acetylcholine synthesis, or to a combination of these factors, and that the results are evidence that acetylcholine is a humoral transmitter involved in the initiation of peristalsis.