McAnelly L, Zakon H H
Department of Zoology, University of Texas at Austin 78712, USA.
J Neurosci. 1996 Jul 15;16(14):4383-8. doi: 10.1523/JNEUROSCI.16-14-04383.1996.
The inactivation kinetics of the Na+ current of the weakly electric fish Sternopygus are modified by treatment with androgens. To determine whether phosphorylation could play a role in this effect, we examined whether activation of protein kinase A by 8 bromo cyclic AMP (8 Br cAMP) altered voltage-dependent properties of the current. Using a two-electrode voltage-clamp procedure, we found no effect of 8 Br cAMP on inactivation kinetics or other voltage-dependent properties of the Na+ current of the electrocytes. However, treatment with 8 Br cAMP did produce a dose-dependent increase in the Na+ current compared with saline controls: 17.6% at 100 microM, 42.4% at 1 mM, and 43.1% at 5 mM. This effect was blocked by 30 microM H89, a PKA inhibitor, indicating that the observed effect was attributable to 8 Br cAMP activation of PKA. We conclude that androgen-induced changes in Na+ current inactivation are not mediated by PKA and suggest that PKA-mediated increases in Na+ current underlie increases in the amplitude of the electric organ discharge observed in social interactions or with changes in water conductance.
雄激素处理会改变弱电鱼裸背电鳗钠电流的失活动力学。为了确定磷酸化是否在此效应中起作用,我们研究了用8-溴环磷酸腺苷(8-Br-cAMP)激活蛋白激酶A是否会改变电流的电压依赖性特性。使用双电极电压钳制程序,我们发现8-Br-cAMP对电细胞钠电流的失活动力学或其他电压依赖性特性没有影响。然而,与生理盐水对照相比,用8-Br-cAMP处理确实使钠电流产生了剂量依赖性增加:100微摩尔时增加17.6%,1毫摩尔时增加42.4%,5毫摩尔时增加43.1%。这种效应被30微摩尔的H89(一种蛋白激酶A抑制剂)阻断,表明观察到的效应归因于8-Br-cAMP对蛋白激酶A的激活。我们得出结论,雄激素诱导的钠电流失活变化不是由蛋白激酶A介导的,并表明蛋白激酶A介导的钠电流增加是社交互动中或水导率变化时观察到的电器官放电幅度增加的基础。