Contribution of Ca^<2+>-Dependent Protein Kinase C in the Spinal Cord to the Development of Mechanical Allodynia in Diabetic Mice(Pharmacology)
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概要
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In this paper, we directly demonstrate, for the first time, the activation of Ca^<2+>-dependent protein kinase C (PKC) in the spinal cord of diabetic mice. In streptozotocin (STZ)-treated (200 mg/kg, i.v.) diabetic mice, hypersensitivity (allodynia) to mechanical stimulation appeared 7 d after STZ injection. This mechanical allodynia was inhibited by intrathecal injection of the PKC inhibitors 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) and calphostin C, but not the protein kinase A inhibitor N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinolinesulfonamide (H-89). The activity of membrane-associated Ca^<2+>-dependent PKC in the spinal cords of STZ-induced diabetic mice was significantly higher than that observed in non-diabetic mice. These results suggest that activation of Ca^<2+>-dependent PKC in the spinal cord, contributes to the mechanical allodynia in the pain associated with diabetic neuropathy.
- 公益社団法人日本薬学会の論文
- 2007-05-01
著者
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Migita Keisuke
Department of Neurophysiology, Hirosaki University Graduate School of Medicine
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Honda Kenji
Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
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Takano Yukio
Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
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Takano Y
Dep. Of Physiology And Pharmacology Fac. Of Pharmaceutical Sciences Fukuoka Univ. Jpn
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Takano Y
Department Of Pharmacology Faculty Of Pharmaceutical Sciences Fukuoka University
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Takano Yukio
Department Of Physiology And Pharmacology Faculty Of Pharmaceutical Sciences Fukuoka University
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Honda Kenji
Department Of Physiology And Pharmacology Faculty Of Pharmaceutical Sciences Fukuoka University
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Honda K
Department Of Physiology And Pharmacology Faculty Of Pharmaceutical Sciences Fukuoka University
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Migita Keisuke
Department Of Neurophysiology Hirosaki University Graduate School Of Medicine
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Hirabara Yasutoshi
Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, J
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KOGUCHI Masako
Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
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KOGA Kohei
Department of Integrative Physiology, School of Medicine, Kyushu University
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NAKAJIMA kyoko
Joint Laboratory for Pathological Biochemistry, School of Medicine. Fukuoka University
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KOBAYASHI Fumito
Department of Physiology and Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
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OGATA Shigenori
Joint Laboratory for Pathological Biochemistry, School of Medicine. Fukuoka University
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Honda K
Dep. Of Physiology And Pharmacology Fac. Of Pharmaceutical Sciences Fukuoka Univ. Jpn
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Nakajima Kyoko
Joint Laboratory For Pathological Biochemistry School Of Medicine. Fukuoka University
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Takano Yukio
Department Of Applied Physics Faculty Of Engineering University Of Tokyo
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Koga Kohei
Department Of Integrative Physiology School Of Medicine Kyushu University
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Koguchi Masako
Department Of Physiology And Pharmacology Faculty Of Pharmaceutical Sciences Fukuoka University
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Honda K
Dep. Of Physiology And Pharmacology Fac. Of Pharmaceutical Sciences Fukuoka Univ.
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Ogata Shigenori
Joint Laboratory For Pathological Biochemistry School Of Medicine. Fukuoka University
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Ogata Shigenori
Joint Laboratory For Pathological Biochemistry Fukuoka University School Of Medicine
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Honda Kenji
Department Of Chemistry Toho University
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Kobayashi Fumito
Department Of Physiology And Pharmacology Faculty Of Pharmaceutical Sciences Fukuoka University
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Hirabara Yasutoshi
Department Of Physiology And Pharmacology Faculty Of Pharmaceutical Sciences Fukuoka University
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Hirabara Yasutoshi
Department Of Pharmacy University Miyazaki Hospital
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Ogata Shigenori
Joint Laboratory For Frontier Medical Science Faculty Of Medicine Fukuoka University
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