Modulatory inputs to trigeminal motoneurons in rat slice preparation

采用细胞内记录法研究了血清素和去甲肾上腺素对三叉神经运动神经元（TMNs）的影响。对3 ~ 6周龄大鼠脑干切片（450 ~ 500 mm厚）的颞叶神经网络进行记录。血清素（20-100 muM）和去甲肾上腺素（40-100muM）在大多数细胞中引起去极化和输入电阻增加。两种药物均增强了随时间变化的内向整流。这些效果在河豚毒素存在的情况下仍然存在。此外，血清素和去甲肾上腺素也增加了每个细胞对注射电流的放电频率反应。去甲肾上腺素增强去极化尖峰后电位（ADP），减弱中期超极化尖峰后电位（mAHP）。另一方面，血清素延缓了mAHP的峰值时间，延长了mAHP的半衰减时间，但对ADP没有影响。上述结果表明，除血清素对mAHP的影响外，去甲肾上腺素和血清素对TMNs活性的影响更大。研究了脉冲后电位的性质。apamin （1muM）和2mM Co^<2+>以及细胞内注射EGTA均可抑制mAHP，这表明产生mAHP的钾电导是由Ca^<2+>内流激活的。2mM Mn^<2+>或500muM Cd^<2+>均可降低ADP，而通过将[Ca^<2+>] 0从2mM提高至8 mM和细胞内注射EGTA可提高ADP振幅。这表明Ca^<2+>本身很可能是产生ADP的载流子。局灶施用omega - concontoxin GVIA （10-30 muM）抑制了mAHP，提高了ADP，而局灶施用omega - agatoxin IVA （10-100 muM）降低了ADP幅度，但对mAHP没有明显影响。我们得出结论，Ca^<2+>通过ω -蛇形毒素iva敏感钙通道内流至少在一定程度上导致了ADP的产生，Ca^<2+>通过ω -蛇形毒素gvia敏感钙通道内流有助于mAHP的产生。少

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