Induction of tolerance to ischemia: Alterations in second-messenger systems in the gerbil hippocampus
Autor: | Kyuya Kogure, Tsutomu Araki, Kenshi Murase, Hiroyuki Kato |
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Rok vydání: | 1992 |
Předmět: |
Male
medicine.medical_specialty Phosphodiesterase Inhibitors Ischemia Hippocampus Biology Gerbil Second Messenger Systems Neuroprotection Brain Ischemia chemistry.chemical_compound Internal medicine Cyclic AMP medicine Animals Inosine Triphosphate Cyclic adenosine monophosphate Inositol phosphate Phorbol 12 13-Dibutyrate Rolipram chemistry.chemical_classification Forskolin General Neuroscience Colforsin medicine.disease Pyrrolidinones Endocrinology chemistry Anesthesia Autoradiography Gerbillinae Protein Kinases medicine.drug |
Zdroj: | Brain Research Bulletin. 29:559-565 |
ISSN: | 0361-9230 |
DOI: | 10.1016/0361-9230(92)90123-f |
Popis: | Preconditioning the brain with sublethal ischemia protects against neuronal damage following subsequent ischemic insult. Using [3H]inositol 1,4,5-triphosphate (IP3), [3H]phorbol 12,13-dibutyrate (PDBu), [3H]forskolin, [3H]cyclic adenosine monophosphate (cAMP) and [3H]rolipram, we performed quantitative autoradiography to determine postischemic alterations in second-messenger systems in the gerbil hippocampus following preconditioning the brain with sublethal ischemia. At 7 days of reperfusion, no alterations were observed in brains subjected to 2 min of forebrain ischemia which produced no neuronal damage. However, 3-min ischemia caused a 75% reduction in [3H]IP3 binding (p < 0.01 vs. control) and 15–25% reductions in [3H]forskolin (p < 0.01 vs. control), [3H]cAMP (p < 0.05 vs. control), and [3H]rolipram (p < 0.01 vs. control) binding in the CA1 subfield coincident with histopathological CA1 pyramidal cell destruction, but no significant alterations in [3H]PDBu binding. Preconditioning the brain with 2 min of ischemia followed by 4 days of reperfusion prevented both histopathological cell death and the reductions in binding following subsequent 3 min of ischemia. Interestingly, [3H]IP3 and [3H]rolipram binding in CA1 showed a transient reduction, by 30% and 20% (both p < 0.01 vs. control), respectively, in the early reperfusion period. This downregulation of the IP3 system may play a role in the protection against cell death. |
Databáze: | OpenAIRE |
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