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在急性分离的豚鼠胃窦平滑肌细胞上 ,利用膜片钳技术的传统全细胞模式记录离子电流的方法 ,探讨微丝在低渗牵张诱导毒蕈碱电流增加中的作用。当豚鼠胃窦平滑肌细胞的膜电位钳制在 - 2 0mV时 ,灌流液中 5 0μmol/L 卡巴胆碱 (carbachol,CCh)或电极内液中 0 5mmol/LGTPγS均可引导毒蕈碱电流 (muscariniccurrentICCh) ,低渗牵张 ( 2 0 2mOsmol/L)分别使其增加 145± 2 7%和 183± 3 0 % ;当电极内液中加入 2 0 μmol/L的细胞松弛B (一种微丝骨架的解聚剂 )时 ,低渗牵张使ICCh只增加 70± 6% ;而电极内液中加入 2 0 μmol/L的鬼笔环肽 (一种微丝骨架的稳定剂 )则使ICCh增加了 5 45± 81%。结果表明 ,低渗牵张可增加由卡巴胆碱或GTPγS诱导的毒蕈碱电流 ,微丝参与调节低渗牵张诱导豚鼠胃窦平滑肌细胞ICCh增加的作用
In acutely isolated guinea pig gastric antral smooth muscle cells, the effect of microfilaments on the increase of muscarinic currents induced by hypotonic stretch distraction was investigated using the traditional whole-cell recording technique of patch clamp technique. When the membrane potential of guinea pig gastric smooth muscle cells was clamped at -2OmV, 50 micromol / L carbachol (CCh) or 0 5 mmol / L LGTPγS in the perfusate could induce muscarinic current ICCh , Hypotonic stretch (2 0 2 mOsmol / L) increased 145 ± 27% and 183 ± 30% respectively. When 20 μmol / L of cytochalasis B (a kind of microfilament skeleton Depolymerization), ICCh increased by only 70 ± 6% with hypotonic stretch, whereas addition of 20 μmol / L phalloidin, a fibril backbone stabilizer, to the electrode solution increased ICCh 5 45 ± 81%. The results showed that hypotonic stretch can increase muscarinic currents induced by carbachol or GTPγS, and actin is involved in the regulation of ICCh increase induced by hypotonic stretch in guinea-pig gastric antral smooth muscle cells