Brain-derived neurotrophic factor prevents neuronal death and glial activation after global ischemia in the rat
| Autor: | Matthias Spranger, Stefan Schwab, Irina Kiprianova, Stephanie Desiderato, Roland Galmbacher, Thomas M. Freiman, Frank Gillardon |
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| Rok vydání: | 1999 |
| Předmět: |
Male
medicine.medical_specialty Ischemia Nitric Oxide Synthase Type II Hippocampus Apoptosis DNA Fragmentation Biology Neuroprotection Cellular and Molecular Neuroscience Neurotrophic factors Internal medicine In Situ Nick-End Labeling medicine Animals Rats Wistar Neurons Brain-derived neurotrophic factor TUNEL assay Brain-Derived Neurotrophic Factor medicine.disease Rats Nitric oxide synthase Neuroprotective Agents Endocrinology nervous system Terminal deoxynucleotidyl transferase Ischemic Attack Transient Nerve Degeneration Reperfusion biology.protein Nitric Oxide Synthase Neuroglia Neuroscience |
| Zdroj: | Journal of Neuroscience Research. 56:21-27 |
| ISSN: | 0360-4012 |
| DOI: | 10.1002/(sici)1097-4547(19990401)56:1<21::aid-jnr3>3.0.co;2-q |
| Popis: | The expression of brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B are both increased after global ischemia. Therefore, a protective action of BDNF against the delayed degeneration of vulnerable neurons has been suggested. We have investigated the neuroprotective action of BDNF in global ischemia induced by a four-vessel occlusion in the rat. Following reperfusion, 0.06 microg/hr BDNF was continuously administered intracerebroventricularly with an osmotic minipump. Rats were sacrificed up to 7 days after ischemia and neuronal degeneration was identified by terminal transferase and biotin-dUTP nick end labeling (TUNEL) staining. Additionally, the glial reaction was investigated immunohistochemically and by measuring the activation of immunological nitric oxide synthase protein expression. Postischemic intracerebroventricular infusion of BDNF prevented neuronal death in the vulnerable CA1 region of the hippocampus. Additionally, astroglial activation and macrophage infiltration, which were observed in association with neuronal death, were inhibited by BDNF. This was paralleled by an inhibition of inducible nitric oxide synthase (iNOS) expression in the hippocampus. Thus, the observed neuroprotective effects of continuous BDNF administration after reperfusion suggest a therapeutic potential for BDNF in cerebral ischemia. |
| Databáze: | OpenAIRE |
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