Sjöstrand F S
Department of Biology, University of California, Los Angeles, CA, USA.
J Submicrosc Cytol Pathol. 2004 Jul-Oct;36(3-4):295-303.
An analysis of image distortion in connection with macular degeneration revealed that seeing objects requires brightness contrast enhancement. Thus macular degeneration changes neural interaction controlling bipolar cell responses to light stimulating photoreceptors to reverse spatial brightness contrast enhancement with the consequence that objects cannot be seen. This shows that the contrast of the retinal images is too low for vision without enhancement. However images consisting of randomly arranged small spots of different brightness are seen because of cones enhancing bipolar cell responses to rod input and rods enhancing bipolar cell responses to cone input. This residual vision and the observation that image distortion disappears at low light intensities reveal that macular degeneration is a functional disorder with intact photoreceptor function. The affection may therefore be caused by a reduction of blood flow through the choriocapillaries associated with ageing. The analysis of image distortion associated with the affection led to a simple way to determine the size of the affected retinal area, making it possible to follow the progression of the affection in a direct and simple way. Basic aspects are described of synaptic interaction within the information processing unit that determines the responses of the bipolar cells to photoreceptor input. This unit is the first information processing unit that has been revealed thanks to the extension of the analysis of the nervous system to the nanometer level at which information is processed. The minute size of the information processing unit, the special conditions for synaptic transmission combined with the short distances separating the synapses create special conditions for neural interaction at the nanometer level, establishing conditions for high speed neural communication.
一项关于与黄斑变性相关的图像失真分析表明,视物需要增强亮度对比度。因此,黄斑变性改变了控制双极细胞对刺激光感受器的光作出反应的神经相互作用,从而使空间亮度对比度增强发生逆转,导致无法视物。这表明,未经增强的视网膜图像对比度对于视觉来说过低。然而,由随机排列的不同亮度的小斑点组成的图像是可见的,这是因为视锥细胞增强了双极细胞对视杆细胞输入的反应,而视杆细胞增强了双极细胞对视锥细胞输入的反应。这种残余视力以及图像失真在低光强度下消失的观察结果表明,黄斑变性是一种光感受器功能完好的功能性疾病。因此,这种病变可能是由与衰老相关的脉络膜毛细血管血流量减少引起的。对与该病变相关的图像失真分析导致了一种确定受影响视网膜区域大小的简单方法,从而能够以直接且简单的方式跟踪病变的进展。文中描述了信息处理单元内突触相互作用的基本方面,该单元决定了双极细胞对光感受器输入的反应。由于将神经系统分析扩展到信息处理的纳米水平,这个单元是首个被揭示的信息处理单元。信息处理单元的微小尺寸、突触传递的特殊条件以及突触之间的短距离,为纳米水平的神经相互作用创造了特殊条件,为高速神经通信奠定了基础。