Finger W
Pflugers Arch. 1983 Apr;397(2):121-7. doi: 10.1007/BF00582049.
Inhibitory postsynaptic membrane channels which are activated by glycine were investigated by means of the noise analysis technique. Dose-response curves were obtained for gamma-aminobutyric acid (GABA) in the presence and in the absence of glycine, and it was concluded that GABA and glycine are likely to activate the same receptors. However, glycine proved to have a very low affinity for the inhibitory postsynaptic receptors; this affinity was smaller than that of GABA by a factor of 1 . 10(3)-2 . 10(3). The mean open time tau of the postsynaptic Cl- channels activated by glycine at E = -100 mV and E = -60 mV membrane potentials were tau = 6.1 ms +/- 1.5 ms and tau = 17.7 ms +/- 2.2 ms, respectively. These values are in agreement with the tau obtained by activation with GABA (Dudel et al. 1980); however, on activation by glycine the potential dependence of tau was larger by a factor of 1.35. At E = -100 mV the conductance gamma of glycine-operated channels was about 3 pS which is a third of the respective conductance elicited by GABA. In the presence of high concentrations of glycine (0.1-0.5 mol/l) spontaneous inhibitory postsynaptic currents (sIPSCs) and 'giant' spontaneous inhibitory postsynaptic currents (gsIPSCs) were observed. Furthermore at high concentrations of glycine an additional glycine-induced noise component was found in the power spectra of current fluctuations at higher frequencies. It was concluded that this spectral component resulted from the closing of otherwise open K+ channels, as has been observed already on application of GABA (Dudel and Finger 1980). The mean duration of the low conductance state was tau- = 2.2 ms +/- 0.9 ms and the conductance decrease gamma- coupled to this process was estimated to be about 3 pS. In Na+ free- and Ca2+-enriched bathing solutions the glycine-induced conductances gamma and gamma- were reduced by a factor of about 1.7 while tau and tau- remained unchanged. The decrease in gamma and gamma- was most likely effected by the increase in concentration of divalent cations.
采用噪声分析技术对由甘氨酸激活的抑制性突触后膜通道进行了研究。在有和没有甘氨酸存在的情况下,获得了γ-氨基丁酸(GABA)的剂量-反应曲线,得出的结论是GABA和甘氨酸可能激活相同的受体。然而,事实证明甘氨酸对抑制性突触后受体的亲和力非常低;这种亲和力比GABA的亲和力小1.10³-2.10³倍。在膜电位E = -100 mV和E = -60 mV时,由甘氨酸激活的突触后Cl⁻通道的平均开放时间τ分别为τ = 6.1毫秒±1.5毫秒和τ = 17.7毫秒±2.2毫秒。这些值与用GABA激活获得的τ值一致(杜德尔等人,1980年);然而,由甘氨酸激活时,τ的电位依赖性大1.35倍。在E = -100 mV时,甘氨酸操作通道的电导γ约为3 pS,这是GABA引起的相应电导的三分之一。在高浓度甘氨酸(0.1-0.5摩尔/升)存在的情况下,观察到自发抑制性突触后电流(sIPSCs)和“巨大”自发抑制性突触后电流(gsIPSCs)。此外,在高浓度甘氨酸时,在较高频率的电流波动功率谱中发现了额外的甘氨酸诱导噪声成分。得出的结论是,这种光谱成分是由原本开放的K⁺通道关闭引起的,这在应用GABA时已经观察到(杜德尔和芬格,1980年)。低电导状态的平均持续时间为τ⁻ = 2.2毫秒±0.9毫秒,与此过程相关的电导降低γ⁻估计约为3 pS。在无Na⁺和富含Ca²⁺的浴液中,甘氨酸诱导的电导γ和γ⁻降低了约1.7倍,而τ和τ⁻保持不变。γ和γ⁻的降低很可能是由二价阳离子浓度的增加引起的。