Nicotinic stimulation of [3H]acetylcholine release from mouse cerebral cortical synaptosomes

J Neurochem. 1984 Dec;43(6):1593-8. doi: 10.1111/j.1471-4159.1984.tb06083.x.


The effects of nicotine and 1,1-dimethyl-4-phenylpiperazinium (DMPP) on the release of newly synthesized [3H]acetylcholine in mouse cerebral cortical synaptosomes were examined. Nicotine and DMPP produced increases in [3H]acetylcholine release, over the level of spontaneous release, of 24% and 30%, respectively, of a maximum depolarization-induced release produced by 50 mM potassium. The maximum effect was achieved at a concentration of 1 X 10(-4) M for both agents. The time course of release indicated a slow onset of action, reaching a maximum effect at 15 min of incubation. Both nicotine and DMPP also produced a slightly greater release of total tritium, measured in the absence of cholinesterase inhibition, than of [3H]acetylcholine. The release induced by nicotine was completely antagonized by hexamethonium and was largely (58%) calcium-dependent. Nicotine also produced an increase in [3H]choline accumulation into synaptosomes. These results indicate that the nicotinic agonists nicotine and DMPP can produce a moderate enhancement of acetylcholine release by a receptor-mediated action on cholinergic nerve terminals in the central nervous system.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholine / metabolism*
  • Animals
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / metabolism*
  • Choline / metabolism
  • Dimethylphenylpiperazinium Iodide / pharmacology*
  • Hexamethonium
  • Hexamethonium Compounds / pharmacology
  • Kinetics
  • Male
  • Mice
  • Nicotine / antagonists & inhibitors
  • Nicotine / pharmacology*
  • Piperazines / pharmacology*
  • Potassium / pharmacology
  • Synaptosomes / metabolism*


  • Hexamethonium Compounds
  • Piperazines
  • Hexamethonium
  • Dimethylphenylpiperazinium Iodide
  • Nicotine
  • Choline
  • Acetylcholine
  • Potassium