| Project/Area Number |
13660292
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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 |
Basic veterinary science/Basic zootechnical science
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
OHTA Toshio Hokkaido Univ. Grad. School of Vet. Med., Asso. Prof., 大学院・獣医学研究科, 助教授 (20176895)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Calcium / enteric neurons / adrenal chromaffin cells / transient receptor potential protein / ion channel / intracellular calcium / タプシガルジン / 細胞内ストア / クロム親和性細胞 / PC12細胞 / オピオイドペプチド / 電位依存性Caチャネル / ミトコンドリア / TRP |
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| Research Abstract |
The main aim of this project was to clarify the regulatory role of capacitative Ca entry mechanisms in enteric neurons. For this purpose the properties of Ca influx pathways and their regulation were examined using chromaffin and PC12 cells as neural models, and cultured enteric neurons. 1) Voltage-dependent Ca channels in chromaffin cells were received an inhibitory control through G-proteins by endogenous opioids. 2) Ca release from the intracellular stores regulated the activity of membrane ionic channels as well as secretory responses. 3) ATP evoked [Ca^<2+>]I increase in enteric neural cells with anti-PGP 9.5-immunoreactivity. After intracellular stored Ca was depleted with ATP and thapsigargin, a sustained [Ca^<2+>]I was produced, which was suppressed by the treatment with SK&F96365, Ni^<2+> and La^<3+>, indicating that the presence of capacitative Ca entry in enteric neuronal cells. 5) RT-PCR revealed that several TRP-proteins, being considered as Ca entry pathways, were expressed in rat brain and enteric neurons. 5) In TRP5-transfected PC12 cells, [Ca^<2+>]I increases induced by stimulation of G-protein coupled receptors such as bradykinin and UTP were significantly larger than those in mock-cells. These results indicate that Ca entry pathways in neural cells were regulated under various mechanisms, and capacitive Ca entry mechanisms play a role as Ca influx pathway stimulated by the neurotransmitters in enteric neurons. Further research is necessarily to elucidate the molecular basis of the channels protein and intracellular regulatory mechanism on capacitative Ca entry in enteric neural cells.
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