Morphine単回投与ラットにおけるNaloxone誘発条件付け場所嫌悪行動に対する扁桃体の関与

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  • 石田 茂
    岡山大学大学院医歯薬学総合研究科臨床薬剤学
  • 下坂 理帆
    岡山大学大学院医歯薬学総合研究科臨床薬剤学
  • 河崎 陽一
    岡山大学病院薬剤部
  • 金 春玉
    岡山大学大学院医歯薬学総合研究科臨床薬剤学
  • 北村 佳久
    岡山大学大学院医歯薬学総合研究科医薬管理学
  • 荒木 博陽
    愛媛大学医学部附属病院薬剤部
  • 千堂 年昭
    岡山大学大学院医歯薬学総合研究科臨床薬剤学 岡山大学病院薬剤部
  • 五味田 裕
    岡山大学大学院医歯薬学総合研究科臨床薬剤学 岡山大学病院薬剤部

書誌事項

タイトル別名
  • Involvement of the Amygdala on Place Aversion Induced by Naloxone in Single-Dose Morphine-Treated Rats
  • Morphine タンカイ トウヨ ラット ニ オケル Naloxone ユウハツ ジョウケン ズケ バショ ケンオ コウドウ ニ タイスル ヘントウタイ ノ カンヨ

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抄録

  Signs characteristic of opiate withdrawal symptoms can be precipitated by an opiate antagonist after short-term infusion or even a single dose of an opiate both in humans and in animals. This phenomenon has been referred to as acute dependence. In contrast to extensive studies on chronic dependence, less is known about the neural mechanisms mediating acute dependence. It will benefit the development of appropriate therapies to facilitate opiate abstinence and reduced craving to better understand the mechanisms underlying acute opiate dependence and to determine whether there are dissociation and similarity between the early and fully developed stages of dependence. In the present study, we examined the influence of c-Fos expression in the amygdala in acquisition of conditioned place aversion (CPA) induced by naloxone-precipitated withdrawal from a single morphine exposure 24 h earlier. The effect of microinjection into the central amygdaloid nucleus (CeA) of various kinds of glutamatergic neurotransmission inhibitors was also investigated. Findings showed that CeA displayed significant increase in c-Fos expression in the acquisition of CPA. Furthermore, CPA was attenuated significantly and dose-dependently by microinjection into CeA of all glutamatergic neurotransmission inhibitors (NMDA receptor antagonist (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclo-hepten-5,10-imine maleate (MK-801), AMPA receptor antagonist 1-(4-aminophenyl)4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine hydrochloride (GYKI52466), metabotropic glutamate receptor antagonist (±)-α-methyl-4-carboxyphenylglycine (MCPG), and glutamate release inhibitor riluzole). These findings suggest that CeA involves the acquisition of CPA induced by naloxone-precipitated withdrawal from a single morphine exposure, and the function of the glutamatergic system projected from the amygdala to nucleus accumbens plays a facilitative role in formation of morphine dependence.<br>

収録刊行物

  • 薬学雑誌

    薬学雑誌 128 (3), 395-403, 2008-03-01

    公益社団法人 日本薬学会

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