Machová J, Kvaltínová Z
Eur J Pharmacol. 1983 Feb 18;87(2-3):277-82. doi: 10.1016/0014-2999(83)90338-2.
The effects of [Leu5]enkephalin and morphine were studied in the cat superior cervical ganglion (SCG) in situ and in vitro. [Leu5]enkephalin induced dose-dependent ganglionic hyperpolarization. Morphine was 50 times less potent than [Leu5]enkephalin in inducing ganglionic hyperpolarization. The effect of [Leu5]enkephalin was antagonized by naloxone in 7 times higher than equimolar doses. It is suggested that the hyperpolarizing effect of [Leu5]enkephalin in the cat SCG could be mediated mainly by delta-opiate receptors. [Leu5]enkephalin in doses inducing dose-dependent hyperpolarization depressed ganglionic transmission by at most 25%. Morphine was 130 times less potent in inducing depression of ganglionic transmission than ganglionic hyperpolarization. [Leu5]enkephalin in the range of doses inducing dose-dependent ganglionic hyperpolarization depressed dose-dependently the stimulus-bound decremental oscillatory potentials evoked by the muscarinic drug McN-A-343. The results indicate that the muscarinic type of ganglionic activity seems to be a more important target for the proposed inhibitory modulatory action of [Leu5]enkephalin than does the nicotinic type of synaptic transmission in the cat SCG.