Modulation of acetylcholine release in rat hippocampus by amino alcohols and Bay K 8644. Academic Article uri icon

Overview

abstract

  • The amino alcohols ethanolamine, R-alaninol and R-prolinol were shown to enhance high potassium evoked release of [3H]acetylcholine from hippocampal slices by monitoring fractional release of tritium during superfusion. This action appeared to be unique to hippocampal cholinergic nerve terminals because R-prolinol did not modulate evoked release of acetylcholine from cortical or striatal slices, dopamine from striatal slices or norepinephrine from hippocampal slices. Bay K 8644, a dihydropyridine activator of calcium L-channels, exhibited a similar specificity profile. Bay K 8644 decreased the EC50 of R-prolinol without changing the maximal response, indicating that the actions of these two compounds converge through a common cellular mechanism. The effect of R-prolinol was blocked by the L-channel antagonists diltiazem and verapamil but not by nifedipine. In contrast, nifedipine only and not diltiazem or verapamil, blocked the enhancement induced by Bay K 8644. It appears then that amino alcohols can modulate the release of acetylcholine in the hippocampus possibly by enhancing calcium entry into nerve terminals through a specific activation of presynaptic L-channels at a site other than that which interacts with dihydropyridines.

publication date

  • November 26, 1993

Research

keywords

  • 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
  • Acetylcholine
  • Ethanolamines
  • Hippocampus
  • Propanolamines
  • Pyrrolidines

Identity

Scopus Document Identifier

  • 0027519598

Digital Object Identifier (DOI)

  • 10.1016/0006-8993(93)90484-5

PubMed ID

  • 7506986

Additional Document Info

volume

  • 629

issue

  • 1