β-endorphin inhibition of endogenous norepinephrine release from the A2 noradrenergic nucleus in vitro: Role of Mu opiate receptors and Na+ ion permeability

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

An in vitro approach was used to determine the opioid receptor subtype mediating β-endorphin inhibition of endogenous norepinephrine release from the A2 nucleus in the caudal dorsomedial medulla of rats. The voltage- sensitive Na+ channel blocker tetrodotoxin was used to investigate the role of Na+-dependent action potentials in β-endorphin inhibition of K+evoked norepinephrine release. Human β-endorphin1-31 inhibited K+-evoked norepinephrine release in a concentration-dependent fashion. Activation of δ and κ-opioid receptors had no effect on endogenous norepinephrine release. The inhibitory effect of β-endorphin was blocked in a concentration- dependent manner by the μ-opioid receptor antagonist CTOP (Cys2, Tyr3, Orn5, Pen7 amide). Tetrodotoxin (TTX) inhibited norepinephrine release evoked by 25 mM K+ in a concentration-dependent manner and blocked the inhibitory effects of β-endorphin. These results indicate that β-endorphin acts on μ-opioid receptors to inhibit K+-evoked norepinephrine release from A2 neurons and suggest that the receptors involved are not located on noradrenergic nerve terminals.

Original languageEnglish
Pages (from-to)19-23
Number of pages5
JournalBrain Research Bulletin
Volume44
Issue number1
DOIs
StatePublished - Jan 1 1997

    Fingerprint

Keywords

  • Brain slices
  • Opioid
  • Solitary nucleus
  • Tetrodotoxin
  • U-50,488
  • [D-Pen,D- Pen]enkephalin

Cite this