Pathogenesis and Evolutional Mechanism of Hypoglycemic Neuronal Death: Immunohistochemical Study on Synaptic Regions of Rat Hippocampus.:Immunohistochemical Study on Synaptic Regions of Rat Hippocampus
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In order to clarify the pathogenesis and evolutional mechanism of hypoglycemic neuronal death, we performed an immunohistochemical study of the rat hippocampus after severe hypoglycemia (isoelectric EEG for 30 min) by the ABC method using monoclonal antibodies against MAP2 (postsynaptic dendritic protein), synaptophysin (presynaptic protein) and GAP43 (presynaptic protein associated with axonal growth, synaptogenesis and neurotransmitter release).<BR>At 30 min after hypoglycemia, MAP2 immunoreactivity was transiently decreased in the lateral CA1 region in which pyramidal cells appeared unchanged. During the period from 2 hours to 7 days after hypoglycemia, neuronal necrosis first appeared in granular cells of the dentate crest and gradually extended from the subiculum and CA1 to CA2 with decreasing MAP2 and increasing GAP 43 immunoreactivity. In the initial stage of this process, GAP 43 immunoreactivity was found in the inner molecular layer (presynaptic regions of granular cells) of the dentate gyms before the granular cells started to undergo necrosis. The area positively stained with GAP 43 gradually extended and the intensity of its immunoreactivity was maximal at day 7, when immunoreactivity was found even around necrotic neurons. The immunoreactivity of synaptophysin after hypoglycemia was almost identical to that of GAP 43 in distribution and temporal profile, although the latter exceeded the former in the intensity of the immunoreactivity.<BR>These results suggest that the evolutional mechanism of hypoglycemic brain damage differs from that of ischemic brain damage and that GAP 43 may play an important role in the development of hypoglycemic neuronal death and in synaptic regeneration after neuronal death.
- 一般社団法人 日本糖尿病学会の論文
一般社団法人 日本糖尿病学会 | 論文
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