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大鼠感觉神经元中大去极化对钙通道电流的激活作用:鸟嘌呤核苷酸和(-)-巴氯芬的影响

Activation of calcium channel currents in rat sensory neurons by large depolarizations: effect of Guanine nucleotides and (-)-baclofen.

作者信息

Dolphin A C, Scott R H

机构信息

Department of Pharmacology, St George's Hospital Medical School, London SW17 0RE, UK.

出版信息

Eur J Neurosci. 1990;2(1):104-8. doi: 10.1111/j.1460-9568.1990.tb00386.x.

Abstract

Calcium channel currents have been recorded from cultured rat sensory neurons at clamp potentials of between -30 and +120 mV. At large depolarizing potentials between +50 and +120 mV, the current was outward. This outward current was shown to be largely due to ions passing through calcium channels, because it was substantially although generally incompletely blocked by Cd2+ (1 mM) and omega-conotoxin (1 microM). Internal GTP-gamma-S (100 microM) and to a lesser extent GTP (1 mM) reduced the amplitude and slowed the activation of the outward, as well as the inward calcium channel current. Baclofen (100 microM) reversibly inhibited both the inward and outward currents. These results suggest that the effect of baclofen and G protein activation on calcium channel currents is not due to a shift in the voltage-dependence of channel availability.

摘要

在钳制电位为-30至+120mV的条件下,已记录到培养的大鼠感觉神经元的钙通道电流。在+50至+120mV的大去极化电位下,电流为外向电流。该外向电流在很大程度上被证明是由于离子通过钙通道所致,因为它基本上(尽管通常不完全)被1mM的Cd2+和1μM的ω-芋螺毒素阻断。胞内100μM的GTP-γ-S以及程度较轻的1mM的GTP可降低外向钙通道电流以及内向钙通道电流的幅度并减缓其激活。100μM的巴氯芬可可逆地抑制内向和外向电流。这些结果表明,巴氯芬和G蛋白激活对钙通道电流的影响并非由于通道可用性电压依赖性的改变。

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