| Project/Area Number |
10671741
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ISHIKAWA Yasuko The Univ.of Tokushima, Sch.of Dentistry, Associate Professor, 歯学部, 助教授 (40144985)
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| Co-Investigator(Kenkyū-buntansha) |
SKOWRONSKI Mariusz The Univ.of Tokushima, Sch.of Dentistry, Research Associate, 歯学部, 助手 (00294702)
IMAI Yasuo The Univ.of Tokushima, Sch.of Dentistry, Research Associate, 歯学部, 助手 (11671843)
ISHIDA Hajime The Univ.of Tokushima, Sch.of Dentistry, Professor, 歯学部, 教授 (70028364)
EGUCHI Takafumi The Univ.of Tokushima, Sch.of Dentistry, Research Associate, 歯学部, 助手 (90263847)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2000: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1998: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Water channel / Aquaporin-5 / Salivary glands / Aging / M3-Muscarinic receptor / α1-Adrenergic receptor / Apical plasma membrane / Intracellular calcium concentration / 管腔膜 / アクアホリン-5 / 細胞内移動 |
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| Research Abstract |
Salivary glands are innovated by the autonomic nerve. The stimulations of muscarinic and a- and b- adrenergic receptors in the tissues activate the salivary secretion. Aquaporin-5 which was cloned from submandibular glands was shown to be localized topographically in the apical plasma membrane (APM) of duct cells in rat parotid glands. In this investigation, to evaluate the role of aquaporin-5 in salivary secretion induced by nervous stimulation, the alteration of the distribution of aquaporin-5 in rat parotid tissues induced by acetylcholine or epinephrine was studied by immunoblot analysis. The treatment of the tissues with acetylcholine or epinephrine within 1 min induced the increase in the amount of aquaporin-5 in APM, but that for more than 10 min resulted in the decrease of the amount of aquaporin-5 in APM.Acetylcholine-induced increase in the amount of aquaporin-5 in APM was inhibited by atropine, p-F-HHSiD and TMB-8, but not by methoctramine, GF-109203X or H-7. A-23187 alone s
… More
timulated the increase in the amount of aquaporin-5 in APM.While, epinephrine-induced increase in the amount of aquaporin-5 in APM was mimicked by phenylephrine, but not by clonidine, dobutamine, or salbutamol. It was inhibited by phentolamine, but not by propranolol. Furthermore, epinephrinethe-induced increase of aquaporin-5 was inhibited by cytochalasin-D and tubulozole-C.These results indicated that acetylcholine and epinephrine acted on M3-muscarinic and al-adrenergic receptors, respectively and induced the increase in the amount of aquaporin-5 in APM, and that [Ca2+]i elevation by acetylcholine or epinephrine may play a key role in this increase. In addition the involvement of the cytoskeleton was shown in these induction.
The increase of the amount of aquaporin-5 in APM by acetylcholine was 3-fold in the tissues of young adult rats, but 2-fold in those of senescent rats. The difference between the amounts of aquaporin-5 in APM in these rats may depend on that between the [Ca2+]i elevated by acetylcholine. Less
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