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首页> 外文期刊>Journal of submicroscopic cytology and pathology >Sequential pictorial presentation of neural interaction in the retina. 2. The depolarizing and hyperpolarizing bipolar cells at rod terminals.
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Sequential pictorial presentation of neural interaction in the retina. 2. The depolarizing and hyperpolarizing bipolar cells at rod terminals.

机译：视网膜中神经相互作用的顺序图示。 2.杆末端的去极化和超极化双极细胞。

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Each rod is connected to one depolarizing and one hyperpolarizing bipolar cell. The synaptic connections of cone processes to each bipolar cell and presynaptically to the two rod-bipolar cell synapses establishes conditions for lateral interaction at this level. Thus, the cones raise the threshold for bipolar cell depolarization which is the basis for spatial brightness contrast enhancement and consequently for high visual acuity (Sjostrand, 2001a). The cones facilitate ganglion cell depolarization by the bipolar cells and cone input prevents horizontal cell blocking of depolarization of the depolarizing bipolar cell, extending rod vision to low illumination. The combination of reduced cone input and transient hyperpolarization of the hyperpolarizing bipolar cell at onset of a light stimulus facilitates ganglion cell depolarization extensively at onset of the stimulus while no corresponding enhancement applies to the ganglion cell response at cessation of the stimulus, possibly establishing conditions for discrimination between on- vs. off-signals in the visual centre. Reduced cone input and hyperpolarization of the hyperpolarizing bipolar cell at onset of a light stimulus accounts for Granit's (1941) 'preexcitatory inhibition'. Presynaptic inhibition maintains transmitter concentration low in the synaptic gap at rod-bipolar cell and bipolar cell-ganglion cell synapses, securing proportional and amplified postsynaptic responses at these synapses. Perfect timing of variations in facilitatory and inhibitory input to the ganglion cell confines the duration of ganglion cell depolarization at onset and at cessation of a light stimulus to that of a single synaptic transmission.
机译：每根杆连接一个去极化和一个超极化双极电池。视锥突与每个双极细胞的突触连接以及与两个杆-双极细胞突触的突触连接为这一水平的横向相互作用建立了条件。因此，视锥细胞提高了双极细胞去极化的阈值，这是增强空间亮度对比度并因此获得高视力的基础（Sjostrand，2001a）。视锥细胞通过双极细胞促进神经节细胞的去极化，而视锥细胞的输入可防止水平细胞阻断去极化双极细胞的去极化，从而将视杆视力延伸至低照度。减少的视锥细胞输入和在光刺激开始时超极化双极细胞的瞬时超极化的组合，在刺激开始时广泛促进神经节细胞去极化，而在刺激停止时没有相应的增强适用于神经节细胞反应，可能为在视觉中心区分开和关信号。发生光刺激时，视锥细胞输入减少和超极化双极细胞的超极化作用是Granit（1941）“兴奋前抑制”的原因。突触前抑制使杆双极细胞和双极细胞-神经节细胞突触处的突触间隙中的递质浓度保持较低，从而确保这些突触处的比例和放大的突触后反应。神经节细胞的促进和抑制性输入变化的最佳时机将神经节细胞去极化的持续时间限制为在开始和停止光刺激时仅持续一次突触传递。

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