CAJ | 학술논문

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-20 mV时, 灌流液中50 μmol/L 卡巴胆碱(carbachol, CCh)或电极内液中0.5 mmol/L GTPγS均可引导毒蕈碱电流(muscarinic current ICCh), 低渗牵张(202 mOsmol/L)分别使其增加145±27%和183±30%; 当电极内液中加入20 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20 μmol/L的鬼笔环肽(一种微丝骨架的稳定剂)则使ICCh增加了545±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.
재급성분리적돈서위두평활기세포상, 이용막편겸기술적전통전세포모식기록리자전류적방법, 탐토미사재저삼견장유도독심감전류증가중적작용.당돈서위두평활기세포적막전위겸제재-20 mV시, 관류액중50 μmol/L 잡파담감(carbachol, CCh)혹전겁내액중0.5 mmol/L GTPγS균가인도독심감전류(muscarinic current ICCh), 저삼견장(202 mOsmol/L)분별사기증가145±27%화183±30%; 당전겁내액중가입20 μmol/L적세포송이B (일충미사골가적해취제)시, 저삼견장사ICCh지증가70±6%; 이전겁내액중가입20 μmol/L적귀필배태(일충미사골가적은정제)칙사ICCh증가료545±81%.결과표명, 저삼견장가증가유잡파담감혹GTPγS유도적독심감전류, 미사삼여조절저삼견장유도돈서위두평활기세포ICCh증가적작용.
To investigate the relationship between cytoskeleton and hyposmotic membrane stretch-induced increase in muscarinic current, the role of actin microfilament in hyposmotic membrane stretch-induced increase in muscarinic current was studied with the whole-cell patch clamp technique in guinea-pig gastric myocytes. In this study, the muscarinic current was induced by carbachol (50 μmol/L) or GTPγS (0.5 mmol/L). The results showed that hyposmotic superfusate (202 mOsmol/L) increased carbachol-induced current (ICCh) by 145±27% and increased GTPγS-induced current by 183±30%; but in the presence of cytochalasin-B (Cyt-B, 20 μmol/L), an actin cytoskeleton disruptor, hyposmotic membrane stretch increased ICCh by 70±6%. However, hyposmotic membrane stretch induced increase in ICCh was potentiated to 545±81% by phalloidin (20 μmol/L), an actin microfilament stabilizer. The results demonstrated that hyposmotic membrane stretch increased the muscarinic currents induced by carbachol or GTPγS and that the actin microfilament is involved in the process in guinea-pig gastric myocytes.