Effect of opioid peptides on electrically evoked acetylcholine release from Torpedo electromotor neurons

Lea Oron, Yosef Sarne, Daniel M. Michaelson*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

The opioid peptide dynorphin A(1-8) (1 μm) increased acetylcholine release from the Torpedo electric organ by approximately twofold. This effect was reversed by the opiate antagonist naloxone. The effect of Dyn A(1-8) on acetylcholine release was found to vary in magnitude with the seasons of the year, with maximal enhancement being observed in the summer and none in winter. Dynorphin B, methionine-enkephalin and leucine-enkephalin also increased acetylcholine release and showed similar seasonal variations. These findings suggest that acetylcholine release from Torpedo electromotor neurons is regulated by opiate receptors. The physiological significance of these observations is discussed in view of the previous findings that the Torpedo neurons contain an endogenous enkephalin-like peptide.

Original languageEnglish
Pages (from-to)231-234
Number of pages4
JournalNeuroscience Letters
Volume125
Issue number2
DOIs
StatePublished - 29 Apr 1991

Funding

FundersFunder number
United States-IsraeBl mattonalS cienceF oundation85/0097

    Keywords

    • Acetylcholine release
    • Dynorphin
    • Enkephalin
    • Opioid receptor
    • Torpedo

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