Effect of Tetrahydro-9-Aminoacridine on Acetylcholine Release in the Rat Hippocampus.
- Author:
Yeong Hwa JOO
1
;
Suk Won KIM
;
Seung Ho RHO
;
Bong Kyu CHOI
Author Information
1. Department of Pharmacology, School of Medicine, Wonkwang University, Iksan, Korea. cbk@wonkwang.ac.kr
- Publication Type:Original Article
- Keywords:
Tacrine;
Acetylcholine;
Nicotine;
Hippocampus
- MeSH:
Acetylcholine*;
Alzheimer Disease;
Animals;
Central Nervous System;
Cholinergic Agents;
Cholinesterases;
Hippocampus*;
Humans;
Learning;
Memory;
Nicotine;
Palliative Care;
Physostigmine;
Rats*;
Receptors, Muscarinic;
Receptors, Nicotinic;
Tacrine
- From:Korean Journal of Psychopharmacology
1999;10(2):173-179
- CountryRepublic of Korea
- Language:English
-
Abstract:
It is well known that the cholinergic innervation of hippocampal formation plays an important role in the process of memory and learning, and the deficit of this system might be a cause of the senile dementia including Alzheimer's disease. Several studies have suggested that increased central cholinergic activity could improve the cognitive deficits of the senile dementia. Therefore, many attempts have been made to reverse theses cognitive impairment by enhancing the central cholinergic activity through the use of cholinomimetics such as ACh precusor, cholinesterase(ChE) inhibitors and direct cholinoceptor agonists. Since Summers et al. reported that tacrine is worthy of novice as a possible palliative treatment for Alzheimer's disease, it has been shown to improve the memory and cognitive functions in some patients. Although tacrine is a potent centrally cholinesterase inhibitor, it seems unlikely that this property alone could underlie its clinical effect. Because the eserine, a specific cholinesterase inhibitor, showed little improvement in such patients, it is possible that tacrine may act in a different way to produce its clinical efforts. There are reports that tacrine blocked the some types of cation channels and the muscarinic receptors, and stimulated the nicotinic receptors in the central nervous system. After all, though a large body of experimental data have been accumulated, the mechanism controlling ACh release be tacrine still remains to be elucidated. In attempt to address the abode issue, this study was designed to delineate the action mechanism of tacrine on the electrically-evoked ACh release in the rat hippocampus.
