Effects of proteoglycans on the membrane dysfunction produced by in vitro ischemia in the rat hippocampal CA1 neurons.
| Project/Area Number |
16590170
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | KURUME UNIVERSITY |
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Principal Investigator |
HIGASHI Hideho Kurume University, Sch Med, Dept Physiol, Professor, 医学部, 教授 (10098907)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Eiichiro Kurume University, Sch Med, Dept Physiol, Associate Professor, 医学部, 助教授 (80188284)
SOTOGAKU Naoki Kurume University, Sch Med, Dept Physiol, Assistant, 医学部, 助手 (60368884)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2004: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Astrocyte / Proteoglycan / Hippocampus / Extracellular K^+ concentration / Cytoplasmic Ca^<2+> concentration / Heparan sulfate / Chondroitin sulfate / Ischemia / 中枢神経系 / CA1錐体細胞 / 脳虚血 / 細胞内情報伝達系 / グリア / 細胞内Ca^<2+>濃度 / 細胞構築 |
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| Research Abstract |
Intracellular recordings made from pyramidal neurons and astrocytes in the rat hippocampal CA1 region revealed that superfusion with oxygen and glucose-deprived medium (in vitro ischemia) produced a rapid depolarization after 6 min of exposure. When oxygen and glucose were reintroduced immediately after the rapid depolarization, the membrane depolarized further, reaching 0 mV (membrane dysfunction) in pyramidal neurons, whereas the membrane was completely restored to the preexposure level in astrocytes. Simultaneous measurements of the extracellular K^+ concentration ([K^+]_o) and the membrane potential in astrocytes showed that the potential changes were similar to the changes in the [K^+]_o during and after the in vitro ischemia, and the peak potential of the rapid depolarization (-43 mV) was similar to the potential calculated by the Nernst equation for K^+ ion (-48 mV). To assess effects of proteoglycans on the membrane dysfunction produced by in vitro ischemia, changes in cytoplas
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mic Ca^<2+> concentration ([Ca^<2+>]_i) from Fura-2/AM loaded slices were also measured. Pretreatment of the slices with polysaccharide lyases acting on heparan sulfate (heparinase II and III, 1 U/ml) or chondroitin sulfate (chondroitinase ABC, 20 mU/ml) did not prevent the generation of the rapid depolarization and the corresponding rapid increase in [Ca^<2+>]_i in CA1 pyramidal neurons. In contrast, the membrane was significantly restored toward the preexposure potential levels after the reintroduction. Heparinase II and III, but not chondroitinase ABC, prolonged the latency of the rapid depolarization and the rapid increase in [Ca^<2+>]_i and completely restored the [Ca^<2+>]_i to the preexposure level after the reintroduction. These results suggest that the potential changes in the astrocytes are reflection of the changes in the [K^+]_o produced by the ischemic exposure. Heparan sulfate and chondroitin sulfate proteoglycan may contribute, at least partially, to the generation of the membrane dysfunction of the CA1 pyramidal neurons produced by in vitro ischemia. Less
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Report
(3 results)
Research Products
(20 results)
