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Control of the Release of [3H]-Acetylcholine from Rat Hippocampal Slices by Aminopyridines and Phencyclidine

  • R. D. Schwarz
  • C. J. Spencer
  • A. A. Bernabei
  • T. A. Pugsley
Part of the Advances in Behavioral Biology book series (ABBI, volume 30)

Abstract

Release of acetylcholine (ACh) resulting from the depolarization of cholinergic nerve terminals appears to involve the movement of specific ions across the nerve membrane. Experimentally, electrical stimulation and veratridine release ACh by increasing the flux of Na+ as shown by their sensitivity to the Na+ channel blocker tetrodotoxin (TTX), while elevated K+ releases ACh by a TTX insensitive mechanism. In addition, all three methods appear to require the presence of extracellular Ca++ in order to release ACh from vesicular stores (3, 9, 11). Electrophysiological data have suggested that blockade of K+ channels will also enhance neurotransmitter release by increasing Ca++ entry or utilization, due to the prolongation of the repolarization period (14).

Keywords

Spontaneous Release Cholinergic Function Nerve Membrane Vesicular Store Cholinergic Nerve Terminal 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • R. D. Schwarz
    • 1
  • C. J. Spencer
    • 1
  • A. A. Bernabei
    • 1
  • T. A. Pugsley
    • 1
  1. 1.Warner-Lambert/Parke-Davis Pharmaceutical ResearchAnn ArborUSA

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