| Project/Area Number |
05044188
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Institution | Tokai University |
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Principal Investigator |
TAMURA Kenji Tokai University, School of Medicine, 医学部, 助教授 (20163686)
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| Co-Investigator(Kenkyū-buntansha) |
WADE Paul r. Columbia University, Anatomy and Cell Biology, 解剖細胞生物学教室, Research A
WOOD Jackie d. The Ohio State University, Department of Physiology, 生物学教室, 主任教授
SCHEMANN Michael Max Plack Institut(Bad Nauheim), 主任研究員
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥8,000,000 (Direct Cost: ¥8,000,000)
Fiscal Year 1994: ¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 1993: ¥4,000,000 (Direct Cost: ¥4,000,000)
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| Keywords | Enteric Nervous System, / Substance P, / Afferent nerve / Sensory Neuron, / Seconel messenger, / G protein, / Calbindin / 直腸 / 胃 / モルモット / 迷走神経 / 骨盤神経 |
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| Research Abstract |
In the present project we intended to test the hypothesis that G-proteins coupled both excitatory receptors of myenteric AH neurons. Intracellular methods of electrical recording were used to investigate the effects of GTP-gamma-s and pertussis toxin (PTX) on sloW EPSPs. as well as excitatory responses to substance P (SP). lmpalements were maintained for 5.5hours to evaluate the effects of PTX.Slow EPSPs and SP responses declined progressively and disappeared after 3.75hrs. Hyperpolarizing after-potentials were unaffected by PTX.GTP-gamma-s injection resulted in a progressive increase in slow EPsP-like behavior. Atter GTP-gamma-s, SP-ioduced depolarization was infinitely prolonged resulting in inability to evoke responses after an initial response. The results are consistent with the involvement of G-protein in coupling excitatory receptors in AH! type 2 neurans. The second purpose of this project was to test the hypothesis that the expression of calbindin immunoreactivity(lR)in distal colonic myenteric neurons can be correlated with their electrophysiological and morphological characteristics. After analysis of calbindin-lR,the precise morphology of NB-labeled neurons was revealed by immunoperoxidase histochemistry. All of the MLP neutons and 13% of SLP neurons were calbindin-lR.AH/Type 2 physiological properties were recorded from 3 SLP neurons not expressing calbindin-lR.Six of the SLP neurons were calbindin-lR,4 had S/type 1 and 2 had neither S/Type l nor AH/type 2 electrical properties. These results suggest that the distribution of calbindin-lR in distal colonic myenteric neurons is different from that in the small intestine in the guinea pig. We conclude that calbindin-lR can be used as an indicator or predictor of neither the morphology nor the electrophysiology of myenteric neurons in the guinea pig distal colon.
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