Graduate Institute of Acupuncture Science, College of Chinese Medicine, China Medical University, Taichung, Taiwan, China.
Acta Pharmacol Sin. 2010 Dec;31(12):1553-63. doi: 10.1038/aps.2010.156. Epub 2010 Nov 1.
to investigate the effects of 2'-hydroxy-4'-methoxyacetophenone (paeonol) on the electrophysiological behavior of a central neuron (right parietal 4; RP4) of the giant African snail (Achatina fulica Ferussac).
intracellular recordings and the two-electrode voltage clamp method were used to study the effects of paeonol on the RP4 neuron.
the RP4 neuron generated spontaneous action potentials. Bath application of paeonol at a concentration of ≥ 500 micromol/L reversibly elicited action potential bursts in a concentration-dependent manner. Immersing the neurons in Co(2+)-substituted Ca(2+)-free solution did not block paeonol-elicited bursting. Pretreatment with the protein kinase A (PKA) inhibitor KT-5720 or the protein kinase C (PKC) inhibitor Ro 31-8220 did not affect the action potential bursts. Voltage-clamp studies revealed that paeonol at a concentration of 500 micromol/L had no remarkable effects on the total inward currents, whereas paeonol decreased the delayed rectifying K(+) current (I(KD)) and the fast-inactivating K(+) current (I(A)). Application of 4-aminopyridine (4-AP 5 mmol/L), an inhibitor of I(A), or charybdotoxin 250 nmol/L, an inhibitor of the Ca(2+)-activated K(+) current (I(K(Ca))), failed to elicit action potential bursts, whereas tetraethylammonium chloride (TEA 50 mmol/L), an I(KD) blocker, successfully elicited action potential bursts. At a lower concentration of 5 mmol/L, TEA facilitated the induction of action potential bursts elicited by paeonol.
paeonol elicited a bursting firing pattern of action potentials in the RP4 neuron and this activity relates closely to the inhibitory effects of paeonol on the I(KD).
研究 2'-羟基-4'-甲氧基苯乙酮(丹皮酚)对巨型非洲蜗牛(Achatinia fulica Ferussac)右顶 4 区(RP4)中央神经元电生理行为的影响。
采用细胞内记录和双电极电压钳技术研究丹皮酚对 RP4 神经元的作用。
RP4 神经元产生自发性动作电位。丹皮酚浓度≥500μmol/L 时,可浓度依赖性地可逆诱发动作电位爆发。将神经元浸泡在 Co(2+)取代的无钙溶液中并不能阻断丹皮酚诱发的爆发。蛋白激酶 A(PKA)抑制剂 KT-5720 或蛋白激酶 C(PKC)抑制剂 Ro 31-8220 预处理并不影响动作电位爆发。电压钳研究表明,浓度为 500μmol/L 的丹皮酚对总内向电流没有明显影响,而丹皮酚减少了延迟整流钾电流(I(KD))和快速失活钾电流(I(A))。应用 4-氨基吡啶(4-AP 5mmol/L),I(A)抑制剂,或霍乱毒素 250nmol/L,I(K(Ca))抑制剂,未能诱发动作电位爆发,而四乙铵氯化物(TEA 50mmol/L),I(KD)阻断剂,成功诱发动作电位爆发。在较低浓度 5mmol/L 时,TEA 促进了丹皮酚诱发的动作电位爆发的诱导。
丹皮酚在 RP4 神经元中诱发爆发式动作电位发放模式,这种活动与丹皮酚对 I(KD)的抑制作用密切相关。