作者: Christina Dahl , Lise Sofie Haug , Bjørn Spilsberg , Jon Johansen , Anne Carine Østvold
DOI: 10.1016/S0197-0186(99)00129-1
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摘要: Abstract Changes in inositol (1,4,5)-trisphosphate (IP3) binding properties and the protein level of IP3 receptor have been reported different pathological conditions brain, e.g. cerebral ischemia, Alzheimer’s disease, Huntingtons disease. We used 4-vessel occlusion model rat brain to investigate effect transient ischemica insults on mRNA level, [3H]IP3 binding. Recirculation periods were limited (1–72 h) avoid development delayed neuronal death. found that levels decreased after damage-inducing ischemia (9 min) hippocampus CA1 CA3 regions. The unaltered tolerance-inducing (3 min). However, was significantly reduced both damage- region. Furthermore, all investigated areas showed a when followed by second ischemic insult (3+8.5 min ischemia). remained constant areas. These results indicate capability particularly vulnerable occurs as an early consequence before are these Structural or conformational changes altering may be necessity pathway leading down-regulation levels, observed others.