Do tetrahydroaminoacridine (THA) and physostigmine restore acetylcholine release in Alzheimer brains via nicotinic receptors?

L. Nilsson, A. Adem, J. Hardy, B. Winblad, A. Nordberg

Research output: Contribution to journalArticlepeer-review

96 Citations (Scopus)

Abstract

In the presence of 9-amino-1, 2, 3,4-tetrahydroacridine (THA) 10-4M or physostigmine 10-4 M, the in vitro3H-Acetylcholine (3H-ACh) release from control cortical slices was significantly reduced. In contrast, THA 10-4 M and physostigmine 10-4 M significantly increased the release of3H-ACh in AD/SDAT brain tissue. This facilitating effect on3H-ACh release was partially blocked (50%) in the presence of the nicotinic antagonist d-tubocurarine 10-6 M indicating a possible interaction via nicotinic receptors. The muscarinic antagonist atropine 10-5 M significantly increased the3H-ACh release both in control and AD/SDAT brains, thus indicating preservation of muscarinic autoreceptors in the AD/SDAT cortical tissue. In receptor competition studies with3H-nicotine,3H-ACh and3H-quinuclidinyl benzilate (3H-QNB) as receptor ligands, THA interfered with both nicotinic and muscarinic receptor ligand binding, while physostigmine had much less effect.

Original languageEnglish
Pages (from-to)357-368
Number of pages12
JournalJournal of Neural Transmission
Volume70
Issue number3-4
DOIs
Publication statusPublished - Sep 1987
Externally publishedYes

Keywords

  • Alzheimer's disease
  • H-Acetylcholine release
  • THA
  • muscarinic receptors
  • nicotinic receptors
  • physostigmine
  • receptor subtypes

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry

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