Cystatin C, a protease inhibitor, in degenerating rat hippocampal neurons following transient forebrain ischemia

Cystatin C, a cysteine protease inhibitor produced by the choroid plexus and found in CSF at high concentrations, may have an important role in brain injury. We used the two-vessel occlusion model with hypotension to induce transient forebrain ischemia (TFI) in rats for 10 min and then examined cyst...

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Bibliographic Details
Published in:Brain research 1995-09, Vol.691 (1), p.1-8
Main Authors: Palm, Donald E., Knuckey, Neville W., Primiano, Michael J., Spangenberger, Anthony G., Johanson, Conrad E.
Format: Article
Language:English
Subjects:
Animals
Astrocytes - physiology
Biological and medical sciences
CA1
Cerebrospinal Fluid Proteins - physiology
Choroid plexus
CSF
Cystatin C
Cystatins - physiology
Cysteine protease inhibitor
Cysteine Proteinase Inhibitors - physiology
Delayed neuronal death
Hippocampus - cytology
Hippocampus - physiology
Immunohistochemistry
Ischemic Attack, Transient - physiopathology
Male
Medical sciences
Nerve Degeneration - physiology
Nerve Tissue Proteins - physiology
Neurology
Prosencephalon - blood supply
Pyramidal Cells - cytology
Pyramidal Cells - physiology
Rats
Rats, Sprague-Dawley
Vascular diseases and vascular malformations of the nervous system
γ-Trace protein
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Summary:Cystatin C, a cysteine protease inhibitor produced by the choroid plexus and found in CSF at high concentrations, may have an important role in brain injury. We used the two-vessel occlusion model with hypotension to induce transient forebrain ischemia (TFI) in rats for 10 min and then examined cystatin C immuno-like reactivity (CC-IR) after 1, 3, 7 and 14 days of recovery. Our results reveal that CC-IR was minimal or absent in the hippocampus of normal and 1 day post-ischemic animals. However, CC-IR was present in CA1 pyramidal cells and a small number of reactive glia of the stratum radiatum (SR) and stratum oriens (SO) at 3, 7 and 14 days post-ischemia. Histological assessment of the hippocampus indicates that CC-IR was localized in morphologically degenerative neurons. This distinct temporal expression of cystatin C in the rat hippocampus is concurrent with delayed neuronal death following TFI. Thus, these results indicate that cystatin C and/or its substrates may be important components of the post-ischemic neurodegenerative and repair process.
ISSN:0006-8993
1872-6240
DOI:10.1016/0006-8993(95)00520-Z