Csernoch L, Huang C L, Szucs G, Kovacs L
Department of Physiology, University Medical School, Debrecen, Hungary.
J Gen Physiol. 1988 Nov;92(5):601-12. doi: 10.1085/jgp.92.5.601.
The effects of tetracaine on charge movements and on antipyrylazo III signals monitoring intracellular delta [Ca2+] were compared in cut frog semitendinosus muscle fibers in a single vaseline gap-voltage clamp. Low tetracaine concentrations (25-40 microM) markedly reduced delta [Ca2+] signals and shifted the rheobase. However, they neither influenced charge movement nor that peak delta [Ca2+] value associated with the contractile threshold. Higher tetracaine concentrations (100-200 microM) partly inhibited charge movements in cut fibers. They separated a steeply voltage-sensitive charge, some of whose features resembled 'q gamma' reported in intact fibers, and whose movement preceded delta [Ca2+] signals at threshold. These findings: (a) directly confirm an earlier suggestion that tetracaine acts on steps in excitation-contraction coupling rather than myofilament activation; (b) show that tetracaine at low concentrations can directly interfere with sarcoplasmic reticular calcium release without modifying charge movement; (c) show that the tetracaine-sensitive charge, first found in intact fibers, also exists in cut fibers; and (d) make it unlikely that tetracaine-sensitive charge transfer is a consequence of Ca2+ release as suggested on earlier occasions.
在单个凡士林间隙电压钳中,比较了丁卡因对离体青蛙半腱肌纤维中电荷移动以及对监测细胞内Δ[Ca2+]的偶氮胂III信号的影响。低浓度丁卡因(25 - 40微摩尔)显著降低了Δ[Ca2+]信号并使基强度发生偏移。然而,它们既不影响电荷移动,也不影响与收缩阈值相关的Δ[Ca2+]峰值。较高浓度丁卡因(100 - 200微摩尔)部分抑制了离体纤维中的电荷移动。它们分离出一种对电压敏感的陡峭电荷,其一些特征类似于完整纤维中报道的“qγ”,并且其移动在阈值时先于Δ[Ca2+]信号。这些发现:(a)直接证实了早期的推测,即丁卡因作用于兴奋 - 收缩偶联步骤而非肌丝激活;(b)表明低浓度丁卡因可直接干扰肌浆网钙释放而不改变电荷移动;(c)表明首先在完整纤维中发现的对丁卡因敏感的电荷在离体纤维中也存在;(d)使得丁卡因敏感电荷转移不太可能像早期所认为的那样是Ca2+释放的结果。