Schwarz W, Fox J M
J Membr Biol. 1977 Sep 15;36(4):297-310. doi: 10.1007/BF01868156.
Ultraviolet radiation irreversibly reduces the sodium permeability in nerve membranes and, in addition, induces a change of the potential dependence of the kinetic parameters of sodium inactivation in the node of Ranvier. This second ultraviolet effect shifts the kinetic parameters of sodium inactivation h infinity (V), alpha h (V), and beta h (V) to more negative potentials (no changes of the slopes of the curves). The amount of the displacement delta V along the potential axis is equal for the three parameters and depends on the ultraviolet dose. It is about delta V = --10 mV after an irradiation dose of 0.7 Ws/cm2 at 280 nm. Both ultraviolet-induced effects depend on membrane potential and on the wavelength of the applied radiation. But while the potential shift is enhanced at more negative holding potentials, the ultraviolet blocking is diminished and vice versa. Further, the ultraviolet-induced potential shift is greater at 260 nm than at 280 nm, whereas a maximum sensitivity of ultraviolet blocking is found at 280 nm. Therefore, the two radiation effects are the result of two separate photoreactions. For explanation of the radiation-induced potential shift it is assumed that ultraviolet radiation decreases the density of negative charges at the inner surface of the nodal membrane. From this hypothesis a value for the inner surface potential psii was derived. --19 mV less than or equal to psii less than or equal to --14 mV.
紫外线辐射会不可逆地降低神经膜中的钠通透性,此外,还会引起郎飞结中钠失活动力学参数的电位依赖性变化。紫外线的这第二种效应会将钠失活的动力学参数h∞(V)、αh(V)和βh(V)移向更负的电位(曲线斜率无变化)。这三个参数沿电位轴的位移量δV相等,且取决于紫外线剂量。在280nm处照射剂量为0.7Ws/cm2后,δV约为-10mV。紫外线诱导的这两种效应均取决于膜电位和所施加辐射的波长。但是,虽然在更负的保持电位下电位偏移会增强,但紫外线阻断作用会减弱,反之亦然。此外,紫外线诱导的电位偏移在260nm处比在280nm处更大,而紫外线阻断的最大敏感性在280nm处发现。因此,这两种辐射效应是两个独立光反应的结果。为了解释辐射诱导的电位偏移,假设紫外线辐射会降低结膜内表面的负电荷密度。基于此假设,得出了内表面电位ψii的值。-19mV≤ψii≤-14mV。