Effects of Brain Temperature on Calmodulin and Microtubuleassociated Protein 2 Immunoreactivity in the Gerbil Hippocampus Following Transient Forebrain Ischemia
| Autor: | Tetsuaki Iwamoto, Yuuki Eguchi, Haruhide Ito, Katsuhiro Yamashita |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Male
medicine.medical_specialty Ischemia Hippocampus chemistry.chemical_element Calcium Biology Gerbil Calcium in biology Body Temperature Brain Ischemia Brain ischemia Prosencephalon Calmodulin Microtubule-associated protein 2 Internal medicine medicine Animals Cytoskeleton medicine.disease Immunohistochemistry Endocrinology nervous system chemistry Neurology (clinical) Gerbillinae Microtubule-Associated Proteins Neuroscience |
| Zdroj: | Journal of Neurotrauma. 14:109-118 |
| ISSN: | 1557-9042 0897-7151 |
| DOI: | 10.1089/neu.1997.14.109 |
| Popis: | Increased intracellular calcium and cytoskeletal damage play a crucial role in neuronal death following injury such as cerebral ischemia. The effect of brain temperature on early intracellular calcium increase and neuronal cytoskeletal damage following cerebral ischemia has not been rigorously investigated. In the current communication we evaluated calmodulin (CaM) and microtubule-associated protein 2 (MAP2) in the same brain section using a double labeling immunohistochemical technique, and obtained evidence that the brain temperature has a significant effect on the early calcium increase and cytoskeletal damage as well as the delayed neuronal death occurring in CA1 sector of the gerbil hippocampus after transient forebrain ischemia. In the normothermia (36.7 degrees C) group, CaM and MAP2 immunoreactivity were markedly decreased within 48 h after ischemia and thereafter dramatic neuronal death (grade 3) was seen in the CA1 sector at 7 days. Mild hypothermia (33.3 degrees C) significantly protected against all these changes, whereas cytoskeletal damage and delayed neuronal death were aggravated by mild hyperthermia (39.7 degrees C). We conclude that mild hypothermia protects the brain against transient forebrain ischemia by reducing early cytoskeletal damage and subsequent neuronal death. |
| Databáze: | OpenAIRE |
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