Patch-clamp electrical recordings of rutaecarpine-induced block of delayed rectifier K current in NG-108-15 neuronal cells

• Main Authors: Pei-Hsuan Lin, 林佩萱
• Other Authors: Sheng-Nan Wu
• Format: Others
• Language: zh-TW
• Published: 2002
• Online Access: http://ndltd.ncl.edu.tw/handle/81732936214744282636

碩士 === 國立中山大學 === 生物醫學科學研究所 === 90 === Abstract In the present study, the effects of rutaecarpine on ionic currents of NG108-15 neuronal cells were studied. Rutaecarpine (2-100 μM) suppressed the amplitude of voltage-dependent K+ outward current (IK(DR)) in a concentration-dependent manner. The IC50 value for rutaecarpine-induced inhibition of IK was 11μM. However, rutaecarpine (20 μM) had little effect on L-type Ca2+ current. IK(DR) present in these cells is sensitive to the inhibition by quinidine and dendrotoxin, yet not by E-4031. Rutaecarpine enhanced the rate and extent of IK(DR) inactivation, although it had no effect on the initial activation phase of IK(DR). Recovery from block by rutaecarpine (5 μM) was fitted by a single exponential with a value of 2.87 s. Cell-attached single-channel recordings revealed that rutaecarpine decreased channel activity over the length of the test potential without altering single-channel amplitude. With the aid of binding scheme, a quantitative description of the actions of rutaecarpine on IK(DR) was provided. Under current-clamp configuration, rutaecarpine also prolonged action potential duration in NG108-15 cells without altering other variables of the action potential. The results clearly show that rutaecarpine is a blocker of the KDR channel. The increase in action potential duration induced by rutaecarpine can be explained mainly by its blocking effects on IK(DR).