[3H]acetylcholine release from rat amacrine-like neurons is inhibited by adenosine A1 receptor activation

Neuroreport. 1998 Nov 16;9(16):3693-8. doi: 10.1097/00001756-199811160-00023.

Abstract

We studied the effect of endogenous adenosine on the release of [3H]acetylcholine ([3H]ACh) in cultures enriched (96.4+/-0.4%) in rat cholinergic amacrine-like neurons, as determined by labeling with an antibody against choline acetyltransferase. A small population of these cells also contained GABA. Using these cultures we observed that both [3H]ACh release, which was largely Ca2+-dependent, and 45Ca2+ influx, evoked by depolarization with 50 mM KCl, were increased when adenosine A1 receptor activation was prevented by removal of endogenous adenosine with adenosine deaminase, or by application of the A1 receptor antagonist DPCPX. Our results indicate that, in cultured rat amacrine-like neurons, the activation of A1 receptors decreases calcium influx and, thereby, inhibits [3H]ACh release.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / metabolism*
  • Adenosine Deaminase / pharmacology
  • Animals
  • Animals, Newborn
  • Calcium Channels / physiology
  • Calcium Radioisotopes / pharmacokinetics
  • Cells, Cultured
  • Choline O-Acetyltransferase / metabolism
  • Electric Stimulation
  • Ion Channel Gating / drug effects
  • Ion Channel Gating / physiology
  • Membrane Potentials / drug effects
  • Membrane Potentials / physiology
  • Potassium Chloride / pharmacology
  • Rats
  • Rats, Wistar
  • Receptors, Purinergic P1 / metabolism*
  • Retina / chemistry*
  • Retina / cytology
  • Retina / enzymology*
  • Tritium
  • Xanthines / pharmacology
  • gamma-Aminobutyric Acid / analysis

Substances

  • Calcium Channels
  • Calcium Radioisotopes
  • Receptors, Purinergic P1
  • Xanthines
  • Tritium
  • gamma-Aminobutyric Acid
  • Potassium Chloride
  • 1,3-dipropyl-8-cyclopentylxanthine
  • Choline O-Acetyltransferase
  • Adenosine Deaminase
  • Acetylcholine