Neural mechanism of lateral inhibition in the retina

采用全细胞膜片钳法记录了蝾螈视网膜视锥细胞对水平细胞的反馈机制。100μM微毒素可消除gaba介导的效应。感受野周围的光照诱发锥体去极化，使锥体钙电流的激活电压（I_< ca>）向负电压偏移。这种效应与Verweij et al.（1996）报道的场效应相似，但I_<Ca>的电流-电压（I-V）关系的位移并不仅仅是场效应所期望的沿电压轴的平行位移，因为即使在比I_<Ca>更正的电压峰值处，环绕照明也会增加Ica。高pH溶液在锥形终端层的聚焦应用增加了I_<Ca>，其方式与环绕照明相似。这些观察结果表明，周围照明降低了锥端区质子浓度的可能性。事实上，在碳酸氢盐缓冲液中加入10mM HEPES或15mM Tris可以增强细胞外溶液的pH缓冲能力，增加I_<Ca>，其中环绕照明没有增加I_<Ca>。CNQX超极化水平细胞（HCs）和增广锥体I_<Ca>。Kainate去极化hc和抑制锥I_<Ca>。在kainite或CNQX的存在下均未见锥体的环绕反应。因此，锥i <Ca>极有可能与hc的膜电压密切相关。从目前的结果，我们提出，一个外部质子介导的反馈环绕抑制外视网膜。质子浓度与HC膜电压关系的调节机制有待阐明。

The feedback mechanism from horizontal cells to cone photoreceptors was investigated by the whole cell patch clamp recording from cones in newt retinal slices. GABA-mediated effect has been removed by 100μM picrotoxin. Illumination of the receptive field surround evoked depolarization in cones and shifted the activation voltage of cone calcium current (I_<Ca>) to negative voltages. This effect appeared similar to what was reported by Verweij et al. (1996) as field effect, but the shift of the current-voltage (I-V) relation of I_<Ca> was not merely the parallel shift along the voltage axis as expected for the field effect, because surround illumination increased Ica even at the voltages more positive than I_<Ca> peak. Focal application of high pH solution to the cone terminal layer increased I_<Ca> in a similar manner as the surround illumination. These observations suggest a possibility that surround illumination lowered the proton concentration in the cone terminal region. In fact, enrichment of the pH buffering capacity of extracellular solution by adding 10mM HEPES or 15mM Tris to the bicarbonate buffer increased I_<Ca>, in which additional I_<Ca> increase by surround illumination was not seen. CNQX hyperpolarized horizontal cells (HCs) and augmented cone I_<Ca>. Kainate depolarized HCs and suppressed cone I_<Ca>. Surround responses of cones were not seen in the presence of either kainite or CNQX. Therefore, it is highly likely that cone I_<Ca> is intimately related to the membrane voltage of HCs. From the present results we propose that an external proton mediates feedback for surround inhibition in the outer retina. The mechanisms regulating proton concentration in relation to HC membrane voltage needs to be elucidated.