Dynorphin A (1–13) Alleviated Stress-Induced Behavioral Impairments in Mice
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- Mamiya Takayoshi
- Department of Chemical Pharmacology, Faculty of Pharmacy, Meijo University
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- Hasegawa Yuya
- Department of Chemical Pharmacology, Faculty of Pharmacy, Meijo University
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- Hiramatsu Masayuki
- Department of Chemical Pharmacology, Faculty of Pharmacy, Meijo University
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抄録
In this study we investigated whether κ-opioid receptor stimulation by dynorphin A (1–13), a potent fragment of endogenous peptide, attenuated repeated stress-induced behavioral impairments in mice. In order to reduce the motivation to escape, mice were preexposed to inescapable electric footshock (day 0), and then dynorphin A (1–13) was administered to mice prior to the stress from the next day for 4 d (days 1–4). Dynorphin A (1–13) (1500 pmol/5 µL intracerebroventricular (i.c.v.)) attenuated the repeated stress-induced escape failures from the shock, and this improvement was inhibited by the pretreatment of nor-binaltorphimine (4.9 nmol/kg subcutaneously (s.c.)), a κ-opioid receptor antagonist. In the neurochemical experiments, we detected an increase in 5-hydroxyindoleacetic acid (5-HIAA) content, but not in serotonin (5-HT) content, and an increase in the 5-HIAA/5-HT ratio was observed in the amygdala of the group with footshock compared with the group without shock. Additionally, the changes in 5-HIAA content and the ratio were reversed by dynorphin A (1–13). However, there were no differences in 5-HT or 5-HIAA content or their ratios in the hippocampus among the three groups. These results suggest that dynorphin might alleviate the stress-induced behavioral impairments accompanied by regulation of the 5-HTergic system in the brain.
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 37 (8), 1269-1273, 2014
公益社団法人 日本薬学会
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詳細情報
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- CRID
- 1390001204632216576
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- NII論文ID
- 130004677531
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC2cbos1Kjug%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 025609814
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- PubMed
- 25087948
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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
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- PubMed
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- 使用不可