Cystatin C expression is increased in the hippocampus following photothrombotic stroke in rat

• Published in: Neuroscience letters 2006-03, Vol.395 (2), p.108-113
• Main Authors: Pirttilae, T J, Pitkaenen, A
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Cystatin C; Cystatins - biosynthesis; Cysteine protease inhibitor; Epileptogenesis; Fluorescent Dyes - toxicity; Focal ischemia; Fundamental and applied biological sciences. Psychology; Glia; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Hippocampus - metabolism; Hippocampus - pathology; Hippocampus - physiopathology; Male; Medical sciences; Microscopy, Confocal; Nerve Degeneration - pathology; Nervous system (semeiology, syndromes); Neuroglia - metabolism; Neurology; Post-stroke epilepsy; Rats; Rats, Sprague-Dawley; Rose Bengal; Rose Bengal - toxicity; Status Epilepticus - etiology; Status Epilepticus - pathology; Status Epilepticus - physiopathology; Stroke - complications; Stroke - pathology; Stroke - physiopathology; Vertebrates: nervous system and sense organs
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2005.10.091

Stroke is a major cause of epilepsy, but the molecular mechanisms underlying post-stroke epileptogenesis are unknown. The expression of cystatin C, a cysteine protease inhibitor, is increased in the hippocampus during status epilepticus (SE)-induced epileptogenesis, and regulates both cell death and birth. To test the hypothesis that increased cystatin C expression represents a common molecular alteration induced by epileptogenic brain insults, we investigated the time course, cellular localization, and association of cystatin C expression with neuronal damage during post-stroke epileptogenesis. Stroke was induced with photothrombosis, which leads to epilepsy in approximately 20–30% of rats. Cystatin C expression was increased in the CA1 area of the hippocampus 4 days after photothrombosis, when the diameter of the lesion was the largest. Double-labeling and confocal analysis indicated that cystatin C was expressed in astrocytes and microglia. Unlike after SE, cystatin C expression did not change in the dentate gyrus. Also, increased cystatin C expression was not associated with neurodegeneration, which was demonstrated as an absence of Fluoro Jade B-positive cells in adjacent sections. The present study provides evidence that cystatin C may be involved in cellular alterations that occur after an epileptogenic insult, not only after SE but also after photothrombotic stroke.