Human post-mortem striatal α4β2 nicotinic acetylcholine receptor density in schizophrenia and Parkinson's syndrome

被引:91
|
作者
Durany, N
Zöchling, R
Boissl, KW
Paulus, W
Ransmayr, G
Tatschner, T
Danielczyk, W
Jellinger, K
Deckert, J
Riederer, P
机构
[1] Univ Int Catalunya, E-08190 Barcelona, Spain
[2] Univ Wurzburg, Dept Psychiat, D-97080 Wurzburg, Germany
[3] State Hosp Neurol & Psychiat, D-3362 Mauer, Germany
[4] Univ Munster, Inst Neuropathol, D-48149 Munster, Germany
[5] Univ Innsbruck, Dept Neurol, A-6020 Innsbruck, Austria
[6] Univ Wurzburg, Inst Forens Med, D-97078 Wurzburg, Germany
[7] PKH, Ludwig Boltzmann Inst Clin Neurobiol, A-1140 Vienna, Austria
[8] Ludwig Boltzmann Inst Aging Res, Vienna, Austria
[9] Geriatr Ctr Wienerwald, Dept Neurobiol, A-1130 Vienna, Austria
关键词
nicotine; alpha 4 beta 2 nicotinic acetylcholine receptors; schizophrenia; Parkinson's syndrome;
D O I
10.1016/S0304-3940(00)01144-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The density of nicotinic alpha 4 beta 2 receptors, which are believed to largely mediate nicotine's effects, has been reported to be decreased in post-mortem hippocampus of patients with schizophrenia. In the present study, using [H-3]cytisine as a radioligand, we observed a significant 30% decrease in post-mortem striatum of patients with schizophrenia (n = 12) as compared to controls (n = 12). A 25% decrease of striatal alpha 4 beta 2 receptor density in patients with Parkinson's syndrome (n = 12) was not significant. As an upregulation of alpha 4 beta 2 receptors has been observed due to nicotine consumption, the beneficial effects of nicotine described in patients with schizophrenia may be partly due to a compensation for a decrease in alpha 4 beta 2 nicotinic acetylcholine receptors. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:109 / 112
页数:4
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