Naloxone enhances the release of acetylcholine from cholinergic interneurons of the striatum if the dopaminergic input is impaired

Brain Res. 1991 Jun 28;552(2):343-5. doi: 10.1016/0006-8993(91)90102-2.

Abstract

Naloxone significantly enhanced the release of radioactive acetylcholine ([3H]ACh) from rat striatal slices loaded with [3H]choline either when the nigrostriatal pathway had been destroyed by 6-hydroxydopamine or when the D2 dopamine receptors had been inhibited by sulpiride. This in vitro study supplies the first neurochemical evidence, that, in addition to D2-receptor-mediated dopaminergic tonic control, there is opiate-receptor mediated presynaptic modulation of striatal ACh release, possibly by endogenous enkephalin released from local neurons. Such modulation occurs under conditions in which the dopaminergic input is impaired.

MeSH terms

  • Acetylcholine / metabolism*
  • Animals
  • Apomorphine / pharmacology
  • Cerebral Ventricles / drug effects
  • Cerebral Ventricles / physiology*
  • Corpus Striatum / drug effects
  • Corpus Striatum / physiology*
  • Dopamine / physiology*
  • Injections, Intraventricular
  • Interneurons / drug effects
  • Interneurons / physiology*
  • Male
  • Naloxone / pharmacology*
  • Neurotoxins / pharmacology*
  • Oxidopamine / administration & dosage
  • Oxidopamine / pharmacology*
  • Rats
  • Rats, Inbred Strains
  • Reference Values
  • Sulpiride / pharmacology

Substances

  • Neurotoxins
  • Naloxone
  • Sulpiride
  • Oxidopamine
  • Apomorphine
  • Acetylcholine
  • Dopamine