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 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.
Original language | English (US) |
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Pages (from-to) | 79-87 |
Number of pages | 9 |
Journal | Brain Research |
Volume | 629 |
Issue number | 1 |
DOIs | |
State | Published - Nov 26 1993 |
Keywords
- Calcium channel
- Diltiazem
- Ethanolamine
- Neurotransmitter release
- R-Prolinol
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Neurology
- Molecular Biology
- Developmental Biology