Ischemia-Related Changes in Galanin Expression in the Dentate Hilar Region after Transient Forebrain Ischemia in Gerbils
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- LEE Hyeon Yong
- School of Biotechnology and Bioengineering, Kangwon National University
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- HWANG In Koo
- Department of Anatomy, College of Medicine, Hallym University
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- KIM Dae Ho
- School of Biotechnology and Bioengineering, Kangwon National University
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- KIM Jung Hwa
- School of Biotechnology and Bioengineering, Kangwon National University
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- KIM Chang Ho
- School of Biotechnology and Bioengineering, Kangwon National University
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- LIM Beong Ou
- Department of Applied Biochemistry, Konkuk University
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- KANG Tae-Cheon
- Department of Anatomy, College of Medicine, Hallym University
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- BANG Kyung Hwan
- National Institute of Crop Science
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- SEONG Nak Sul
- National Institute of Crop Science
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- LEE Hak Ju
- Forest Research Institute
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- KIM Jong Dai
- School of Biotechnology and Bioengineering, Kangwon National University
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- WON Moo Ho
- Department of Anatomy, College of Medicine, Hallym University
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Although galanin (GAL) protects hippocampal neurons from ischemic damage, no study has examined ischemia-related changes in endogenous GAL in the hippocampal dentate gyrus. We investigated the chronological changes of GAL, well-known as the potassium channel opener, expression in the dentate gyrus at various times after 5 min of transient forebrain ischemia in gerbils. A few GAL-immunoreactive (IR) neurons were found in the polymorphic layer of the sham-operated group. Three hours after ischemia-reperfusion, the pattern of GAL immunoreactivity was similar to that of the sham-operated group and the number of GAL-IR neurons and immunoreactivity were highest 12 h after ischemic insult. At this time, GAL-IR neurons in the polymorphic layer showed strong GAL immunoreactivity. Thereafter, GAL-IR neurons and immunoreactivity significantly decreased in the dentate hilar region. Four days after ischemic insult, GAL-IR neurons were not detectable. In addition, the results of a Western blot study showed a pattern of GAL expression similar to the immunohistochemical changes. GAL protein content also was highest 12 h after ischemia. In conclusion, the increased expression of endogenous GAL in the dentate gyrus after ischemia is related to response to the ischemic damage.<br>
収録刊行物
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- Experimental Animals
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Experimental Animals 54 (1), 21-27, 2005
公益社団法人 日本実験動物学会
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詳細情報 詳細情報について
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- CRID
- 1390282680019977344
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- NII論文ID
- 10014317298
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- NII書誌ID
- AA11032321
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- COI
- 1:CAS:528:DC%2BD2MXjtVyisLs%3D
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- ISSN
- 18817122
- 00075124
- 13411357
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- NDL書誌ID
- 7228465
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- PubMed
- 15725678
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 使用不可