Golcich M A, Morgan I G, Dvorak D R
Visual Sciences Group, Research School of Biological Sciences, Australian National University, Canberra City, A.C.T.
Brain Res. 1990 Dec 10;535(2):288-300. doi: 10.1016/0006-8993(90)91612-k.
When ganglion cell responses were recorded from optic axons in the superficial layers of the chicken optic tectum, the responses recorded are predominantly ON-OFF transient, with some ON transient, and rare OFF transient responses. Several weeks after excitotoxic lesion of the retina with 40 nmol of kainic acid injected intravitreally, only ON transient responses could be recorded from the contralateral optic tectum. ON response latency and threshold were not affected. At low light intensities responses in the kainic acid-lesioned retinas showed a sustained component which was not detected in control retinas, but at high light intensities, the sustained component disappeared and the responses were extremely transient. The disappearance of the OFF responses seems to be due to elimination of the OFF component of the responses of cells which are normally ON-OFF transient, rather than the silencing of these cells, leaving only the normally ON transient cells. Morphological evidence suggests that approximately two thirds of the bipolar cells and most amacrine cells are destroyed by the kainic acid lesion (Ingham and Morgan, Neuroscience, 9 (1983) 165-181), and pharmacological logic (Morgan, Prog. Retinal Res., 2 (1983) 247-266) suggests that the missing bipolar cells should be OFF bipolar cells. These results therefore suggest that ON-OFF transient cells receive direct input from bipolar cells, which determines their basic response type. These results also suggest that amacrine cells have little if any role to play in the generation of the basic centre responses of these ON-OFF transient ganglion cells, and that while amacrine cells may have a role in the generation of transient responses in the inner plexiform layer, transient responses can be generated without the intervention of amacrine cells, particularly at high intensities.
当从鸡视顶盖浅层的视神经轴突记录神经节细胞反应时，记录到的反应主要是开-关瞬态反应，伴有一些开瞬态反应，而关瞬态反应很少见。在玻璃体内注射40 nmol海人酸对视网膜进行兴奋性毒性损伤几周后，仅能从对侧视顶盖记录到开瞬态反应。开反应的潜伏期和阈值未受影响。在低光照强度下，海人酸损伤的视网膜中的反应表现出一种在对照视网膜中未检测到的持续成分，但在高光照强度下，持续成分消失，反应极其短暂。关反应的消失似乎是由于消除了正常情况下为开-关瞬态的细胞反应的关成分，而不是这些细胞沉默，仅留下正常的开瞬态细胞。形态学证据表明，约三分之二的双极细胞和大多数无长突细胞被海人酸损伤破坏（英厄姆和摩根，《神经科学》，9（1983）165 - 181），药理学逻辑（摩根，《视网膜研究进展》，2（1983）247 - 266）表明缺失的双极细胞应为关双极细胞。因此，这些结果表明，开-关瞬态细胞接受来自双极细胞的直接输入，这决定了它们的基本反应类型。这些结果还表明，无长突细胞在这些开-关瞬态神经节细胞的基本中心反应的产生中几乎没有作用，并且虽然无长突细胞可能在神经节细胞内网状层瞬态反应的产生中起作用，但瞬态反应可以在没有无长突细胞干预的情况下产生，特别是在高强度时。
