Magazanik L G, Snetkov V A, Giniatullin R A, Khazipov R N
Sechenov Institute of Evolutionary Physiology and Biochemistry, Leningrad, U.S.S.R.
Neurosci Lett. 1990 Jun 8;113(3):281-5. doi: 10.1016/0304-3940(90)90598-4.
Bath application of 0.5 and 2 microM acetylcholine (ACh) slowed the decay phase of miniature endplate currents (MEPC) recorded in isolated, voltage-clamped and prostigmine-treated frog sartorius muscle. Washout of ACh led to a decrease of the decay time constant of the MEPC to 72 +/- 5% (n = 5) and 51 +/- 3% (n = 6) of initial values, respectively, followed by very slow and incomplete recovery. MEPC amplitude changed slightly and recovered relatively fast. This discrepancy in the recovery rates is suggested to be due to a 'trapping' ability of desensitized receptors which can compete with the free receptors for ACh molecules and prevent repetitive binding. Thus the high affinity of desensitized receptors to ACh may partially compensate the absence of acetylcholinesterase activity.
在分离的、电压钳制且经新斯的明处理的青蛙缝匠肌中,浴用0.5微摩尔/升和2微摩尔/升的乙酰胆碱(ACh)减缓了微小终板电流(MEPC)的衰减期。洗脱ACh后,MEPC的衰减时间常数分别降至初始值的72±5%(n = 5)和51±3%(n = 6),随后恢复非常缓慢且不完全。MEPC幅度变化轻微且恢复相对较快。这种恢复速率的差异被认为是由于脱敏受体的“捕获”能力,其可与游离受体竞争ACh分子并阻止重复结合。因此,脱敏受体对ACh的高亲和力可能部分补偿了乙酰胆碱酯酶活性的缺失。