Abstract
Using stroke-prone spontaneously hypertensive rats with permanent occlusion of the middle cerebral artery (MCA), we investigated whether the secondary thalamic degeneration following cortical infarction is related to apoptosis, and whether the protein synthesis inhibitor cycloheximide (CHX) ameliorates this degenerative process. TdT-mediated dUTP-biotin nick end labeling (TUNEL staining) revealed a distinct pattern of nuclear staining in many ventroposterior (VP) thalamic nucleus neurons on the lesioned side at 1 week after MCA occlusion. In rats with a single or continuous intraventricular infusion of CHX, starting just after brain ischemia, in the VP thalamic neurons were significantly more numerous than those in the thalamic nucleus of rats with vehicle infusion at 1 week after MCA occlusion. However, at 2 weeks after MCA occlusion, the numbers of VP thalamic neurons were similar in the CHX- and vehicle-treated groups. These findings suggest that the secondary thalamic degeneration following cortical infarction is an event reminiscent of apoptosis and that CHX prevents the secondary thalamic neuronal death transiently.
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