Nägga K, Bogdanovic N, Marcusson J
Department of Geriatric Medicine, University Hospital of Linköping, Sweden.
J Neural Transm (Vienna). 1999;106(11-12):1141-9. doi: 10.1007/s007020050230.
The presynaptically located gamma-aminobutyric acid (GABA) transporter (GAT-1) was studied in a group of patients with Alzheimer's disease (AD) and in a control group using the GAT-1 selective radioligand [3H]tiagabine. Post mortem brain tissue from frontal cortex, temporal cortex, and caudate nucleus from 18 AD patients and 23 age-matched controls were studied. The binding was saturable (Kd 26 nM) and region specific. There were no significant differences between the groups with respect to the binding capacity (Bmax) and binding affinity (Kd). The unaltered [3H]tiagabine binding to GAT-1 protein indicates that intrinsic GABA neurons are spared in Alzheimer's disease.
使用GAT-1选择性放射性配体[3H]噻加宾,对一组阿尔茨海默病(AD)患者和一个对照组的突触前定位γ-氨基丁酸(GABA)转运体(GAT-1)进行了研究。对18例AD患者和23例年龄匹配的对照者的额叶皮质、颞叶皮质和尾状核的死后脑组织进行了研究。该结合具有饱和性(解离常数Kd为26 nM)且具有区域特异性。两组在结合容量(最大结合量Bmax)和结合亲和力(解离常数Kd)方面无显著差异。[3H]噻加宾与GAT-1蛋白的结合未改变,表明在阿尔茨海默病中内在GABA神经元未受影响。