1996 Fiscal Year Final Research Report Summary
Modulatory inputs to trigeminal motoneurons in rat slice preparation
| Project/Area Number |
07838018
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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 | 時限 |
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| Research Field |
咀嚼
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| Research Institution | Osaka University |
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Principal Investigator |
INOUE Tomio Osaka University, Faculty of Dentistry, Assistant Professor, 歯学部, 講師 (70184760)
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| Co-Investigator(Kenkyū-buntansha) |
WAKISAKA Satoshi Osaka University, Faculty of Dentistry, Associate Professor, 歯学部, 助教授 (40158598)
MATSUO Ryuji Osaka University, Faculty of Dentistry, Associate Professor, 歯学部, 助教授 (30157268)
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| Project Period (FY) |
1995 – 1996
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| Keywords | Trigeminal / Motoneuron / Intracelluar recording / In vitro / Serotonin / Noradrenaline / Afterpotential / Calcium ion |
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| Research Abstract |
The effects of serotonin and noradrenalline on trigeminal motoneurons (TMNs) were investigated by using intracellular recording in slice preparation in vitro. Recordings were made from TMNs in the brainstem slices (450-500 mum thick) of rats (3-6 weeks old). Bath application of serotonin (20-100 muM) and noradrenaline (40-100muM) caused depolarization and increased input resistance in the most cells tested. Both drugs enhanced time-dependent inward rectification. These effects persisted in the presence of tetrodotoxin. In addition, serotonin and noradrenerline also increased firing frequency response to injected current in every cell tested. Noradrenaline enhanced the depolarizing spike-afterpotential (ADP) and attenuated the medium-duration hyperpolarizing spike-afterpotential (mAHP). On the other hand, serotonin delayd the peak time of mAHP and prolonged the half decay time of the mAHP but did not affect the ADP.These results indicate noradrenaline and serotonin have excitatory effec
… More
ts on activities of TMNs except for the effects of serotonin on the mAHP.
Properties of spike afterpotential were also investegated. The mAHP was suppressed by bath application of apamin (1muM) and 2mM Co^<2+> and also by intracellular injection of EGTA,suggesting that the potassium conductance generating the mAHP is activated by Ca^<2+> influx. 2mM Mn^<2+> or 500muM Cd^<2+> reduced the ADP while the ADP amplitude was increased by raising [Ca^<2+>] o from 2 to 8 mM and by intracellular injection of EGTA.This would suggest that Ca^<2+> themselves are likely to be the charge carriers generating the ADP.Focal application of omega conotoxin GVIA (10-30 muM) suppressed the mAHP and enhanced the ADP,whereas focal application of omega agatoxin IVA (10-100 muM) reduced the ADP amplitude without apparent effects on the mAHP.We conclude that Ca^<2+> influx through omega agatoxin IVA-sensitive calcium channels is at least in part responsible for the generation of the ADP and that Ca^<2+> influx through omega conotoxin GVIA-sensitive calcium channels contributes to the generation of the mAHP. Less
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