Apoptosis and c-Jun in the thalamus of the rat following cortical infarction.
Cortical infarction produces secondary neuronal damage in the thalamus. In this study we examined the thalamus of the rat following 2 h occlusion of the middle cerebral artery (MCA), and found degeneration and gliosis in the ipsilateral ventropostero-medial thalamic nucleus in those rats that showed cortical infarction 7 and 14 days after occlusion. This was accompanied by isolated cells with fragmented DNA, as revealed by in situ labelling of nuclear DNA fragmentation, and showing morphological features of apoptosis, i.e. chromatin condensation, extreme nuclear shrinkage and apoptotic bodies. In addition, cells immunoreactive for c-Jun showing morphological signs of apoptosis were observed. These results provide evidence of apoptosis in the ipsilateral thalamus following cortical infarction, and suggest that c-Jun is involved in this process.
Soriano
M A
MA
Department de Farmacologia i Toxicologia, CID-CSIC, Hospital Prínceps d'Espanya, Universitat de Barcelona, Spain.
Ferrer
I
I
Rodríguez-Farré
E
E
Planas
A M
AM
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002545:Brain Ischemia / Q000378:metabolism / Q000473:pathology; D002536:Cerebral Arteries / Q000502:physiology; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology; D002544:Cerebral Infarction / Q000378:metabolism* / Q000473:pathology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D016755:Proto-Oncogene Proteins c-jun / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013788:Thalamus / Q000378:metabolism* / Q000473:pathology*
D005904:Glial Fibrillary Acidic Protein; D016755:Proto-Oncogene Proteins c-jun