Journal of Neural Transmission

, Volume 70, Issue 3, pp 357–368

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


  • L. Nilsson
    • Department of PharmacologyUniversity of Uppsala
  • A. Adem
    • Department of PharmacologyUniversity of Uppsala
  • J. Hardy
    • Department of BiochemistrySt. Mary's Hospital Medical School
  • B. Winblad
    • Department of Geriatric Medicine, Karolinska InstituteHuddinge Hospital
  • A. Nordberg
    • Department of PharmacologyUniversity of Uppsala
Short Note

DOI: 10.1007/BF01253610

Cite this article as:
Nilsson, L., Adem, A., Hardy, J. et al. J. Neural Transmission (1987) 70: 357. doi:10.1007/BF01253610


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.

Key words

Alzheimer's disease3H-Acetylcholine releaseTHAphysostigminenicotinic receptorsmuscarinic receptorsreceptor subtypes

Copyright information

© Springer-Verlag 1987