کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4333408 | 1292930 | 2006 | 5 صفحه PDF | دانلود رایگان |
The present study investigated the role of lysosomal enzymes in excitotoxic neuronal damage induced by excessive stimulation of non-NMDA glutamate receptors with kainic acid (KA). Internucleosomal DNA fragmentation was induced after intrastriatal administration of KA 1.25–5.0 nmol to rats. Increased expression of cathepsin B (P < 0.01, n = 6) but not cathepsin L in KA-injected striatum was observed 12 to 24 h after intrastriatal infusion of KA (2.5 nmol). Treatment with intrastriatal infusion of the cathepsin B inhibitor Z-FA-FMK (5–10 μg) 10 min prior to or 3 h after KA injection robustly attenuated KA-induced (2.5 nmol) DNA fragmentation. Z-FA-FMK (10 μg) also significantly reduced the size of striatal lesions induced by KA (P < 0.01, n = 6). These results suggest that lysosomal enzyme cathepsin B plays an important role in excitotoxic neuronal injury.
Journal: Brain Research - Volume 1071, Issue 1, 3 February 2006, Pages 245–249