Witkovsky P, Stone S, Ripps H
Brain Res. 1985 Feb 25;328(1):111-20. doi: 10.1016/0006-8993(85)91329-0.
The light-evoked responses of Müller (glial) cells were monitored by intracellular recording in the isolated, superfused retina of Xenopus laevis. Müller cells had dark resting potentials of -88.5 +/- 6.9 mV and small 1-2 mV light responses of variable waveform in normal Ringer's solution. Exposure to picrotoxin (0.5-1.0 mM) greatly enhanced the light response which then consisted of depolarizing transients (Vmax 5-15 mV) at stimulus onset and offset. GABA (5-10 mM) antagonized the picrotoxin effect and suppressed the light response, whereas 2-amino 4-phosphonobutyrate (0.10-0.15 mM) blocked selectively the 'on' transient. None of these agents appreciably modified the glial cells resting potential level. On the other hand, veratrine (6-9 micrograms/ml) depolarized the Müller cell by 4-13 mV and slowed and greatly reduced the light response. These effects were antagonized by tetrodotoxin (1-4 microM) which itself reduced the light response by 30-50% without altering its shape. On the basis of these findings, we suggest that alterations in the activity of the inner retinal neurons, i.e. amacrine and ganglion cells, are primarily responsible for the drug-induced changes in the membrane potential and light-evoked responses of the Müller cell.
在非洲爪蟾分离的、灌流的视网膜中,通过细胞内记录监测米勒(神经胶质)细胞的光诱发反应。在正常林格氏液中,米勒细胞的静息电位为-88.5±6.9mV,对光的反应较小,为1-2mV,波形可变。暴露于印防己毒素(0.5-1.0mM)可大大增强光反应,此时光反应在刺激开始和结束时由去极化瞬变组成(最大电压5-15mV)。γ-氨基丁酸(5-10mM)可拮抗印防己毒素的作用并抑制光反应,而2-氨基-4-膦酰丁酸(0.10-0.15mM)可选择性阻断“开”瞬变。这些药物均未明显改变神经胶质细胞的静息电位水平。另一方面,藜芦碱(6-9微克/毫升)使米勒细胞去极化4-13mV,减慢并大大降低了光反应。这些效应被河豚毒素(1-4微摩尔)拮抗,河豚毒素本身可使光反应降低30-50%,但不改变其形状。基于这些发现,我们认为视网膜内层神经元,即无长突细胞和神经节细胞活动的改变,是药物诱导米勒细胞膜电位和光诱发反应变化的主要原因。