Modulatory inputs to trigeminal motoneurons in rat slice preparation

大鼠切片制备中三叉神经运动神经元的调节输入

• 批准号: 07838018
• 负责人: INOUE Tomio
• 金额: $ 1.66万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1996
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07838018/
• 关键词: Trigeminal; Motoneuron; Intracelluar recording; In vitro; Serotonin; Noradrenaline; Afterpotential; Calcium ion; 三叉神経運動核; ラット; 細胞内記録

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

采用细胞内记录法研究了5-羟色胺和去甲肾上腺素对离体三叉神经运动神经元（TMN）的作用。从大鼠（3-6周龄）脑干切片（450-500 μ m厚）中的TMN进行记录。浴应用5-羟色胺（20-100 μ M）和去甲肾上腺素（40- 100 μ M）引起去极化和增加的输入电阻在大多数细胞测试。这两种药物都增强了时间依赖性内向整流。这些影响持续存在的河豚毒素。此外，5-羟色胺和去甲肾上腺素也增加了每个测试细胞对注入电流的放电频率反应。去甲肾上腺素增强去极化锋电位（ADP），减弱超极化锋电位（mAHP）。5-羟色胺使mAHP的峰值时间延迟，半衰减时间延长，但对ADP无明显影响，提示去甲肾上腺素和5-羟色胺具有兴奋作用。 ...更多信息 除5-羟色胺对mAHP的影响外，还观察了TMN的放电特性。在水浴中应用apamin（1 μ M）和2 mM Co^<2+>以及细胞内注射EGTA都能抑制mAHP，这表明产生mAHP的钾电导被Ca^<2+>内流激活。2 mM Mn^<2+>或500 μ M Cd^<2+>使ADP降低，而将[Ca^<2+>] o从2提高到8 mM和胞内注射EGTA则使ADP振幅增加，这表明Ca^<2+>本身可能是产生ADP的电荷载体。（10-30 μ M）抑制mAHP并增强ADP，而重点应用欧米茄曲霉毒素IVA（10-100 μ M）降低ADP的幅度，但对mAHP没有明显影响。敏感性钙通道至少部分负责ADP的产生，并且通过ω芋螺毒素GVIA敏感性钙通道的Ca^2+内流有助于mAHP的产生。少

项目成果

井上富雄: "三叉神経運動ニューロンに対するノルアドレナリン入力の影響" 歯科基礎医学会雑誌. 38. 195- (1996)

Tomio Inoue：“去甲肾上腺素输入对三叉神经运动神经元的影响”日本基础牙科医学会杂志 38. 195-（1996）。

T.Morimoto et al.: "Brain and Oral Functions" Elsevier, 10 (1995)

T.Morimoto 等人：“大脑和口腔功能”Elsevier，10 (1995)

Kobayashi, M: "Ionic mechanisms of rat trigeminal motoneurons in vitro" 4th IBRO World Congress of Neuroscience. 322 (1995)

Kobayashi, M：“体外大鼠三叉神经运动神经元的离子机制”，第四届 IBRO 世界神经科学大会。

Inoue, T: "Effects of noradrenerline on rat trigeminal motoneurons" Jpn. J. Physiol.46. S140 (1996)

Inoue, T：“去甲肾上腺素对大鼠三叉神经运动神经元的影响”Jpn。

Kobayashi, M.: "Role of calcium conductances onspike afterpotentials in rat trigemind motoneurons" J. Neurophysiol.(in press). (1997)

Kobayashi, M.：“钙电导对大鼠三叉神经运动神经元尖峰后电位的作用”J. Neurophysiol.（出版中）。