@article{oai:iwatemed.repo.nii.ac.jp:00008715,
 author = {川崎, 敏 and カワサキ, サトシ and 佐々木, 和彦 and ササキ, カズヒコ and KAWASAKI, Satoshi and SASAKI, Kazuhiko},
 journal = {岩手女子看護短期大学紀要, Bulletin of Iwate College of Nursing},
 month = {Jul},
 note = {In Aplysia abdominal ganglion cells, application of 5-hydroxytriptamine (5HT) prolongs the spike duration evoked by artificial depolarizing pulses in the presence of tetraethylammonium chloride (TEA). In contrast, it does not alter the spike duration in normal perfusing media. In attempt to clarify this lack of effect of 5HT in the normal media, voltage clamp method was used. Application of 5HT induced slow voltage-dependent inward current carried by Na+ in the cells clamped at resting level. Furthermore, 5HT augmented a transient inward current followed by slow outward current response elicited by depolarizing pulse from resting level to + 10mV. Application of 10mM TEA markedly depressed the outward current component without affecting the fast inward component, indicating the outward current component sensitive to TEA to be mainly Ca^<2+>-activated K^+-current. In the presence of TEA, 5HT rather depressed the remaining outward current component and shifted the maximum level to inward. The apparent inward shift of the outward current by 5HT was inhibited by Cd^<2+>, a typical Ca^<2+>-channel blocker, suggesting the inward shift was due to increase in Ca^<2+<-current. Further-more, 5HT-induced augmentation of the outward current was not observed in the presence of Cd^<2+> alone dissolved in normal media. These results suggested that 5HT facilitate the opening f voltage-dependent Cd^<2+>_channel, causing an increase in Cd^<2+>_current, and subsequently enhancing the TEA-sensitive Cd^<2+>_activated K^+-current. Our model explains why 5HT in normal media lacks the prolonging effect on the spike duration.},
 pages = {29--36},
 title = {脱分極で発生する外向き電流に対するセロトニンの増強効果},
 volume = {1},
 year = {1994}
}