Agarwala S, Kalil R E
Center for Neuroscience, University of Wisconsin, Madison 53706, USA.
J Comp Neurol. 1998 Mar 9;392(2):252-63. doi: 10.1002/(sici)1096-9861(19980309)392:2<252::aid-cne7>3.0.co;2-1.
Following a unilateral lesion of the visual cortex (cortical areas 17, 18, and 18a) in adult rats, neurons in the ipsilateral dorsal lateral geniculate nucleus (LGN) are axotomized, which leads to their atrophy and death. The time course of this neuronal degeneration was studied quantitatively, and the astroglial response was examined with glial fibrillary acidic protein immunohistochemistry. More than 95% of the neurons in the ipsilateral LGN survive during the first 3 days following a lesion of the visual cortex. However, in the next 4 days, massive neuronal death ensues, reducing the number of surviving neurons to approximately 33% of normal by the end of the first postoperative week. Between 2 weeks and 24 weeks postoperatively, the number of neurons present in the LGN declines very gradually from 34% to 17% of normal. Three days after a lesion of the visual cortex, the mean cross-sectional areas of ipsilateral LGN neurons are 13% smaller than normal (87%). By 1 week after the operation, surviving LGN neurons have atrophied to 66% of their normal area. Subsequently, the size of surviving neurons declines slowly to approximately 50% of normal at 24 weeks after the cortical lesion. Astrocytes in the ipsilateral LGN also react to cortical damage. At 1 day after a lesion of the visual cortex, glial fibrillary acidic protein immunoreactivity in the LGN is almost undetectable, but a distinct increase in immunoreactivity is seen at 3 days. Immunoreactivity peaks between 1 week and 2 weeks postoperatively and, thereafter, remains intense for at least 24 weeks. Thus, following a lesion of the visual cortex, the somata of neurons in the LGN remain essentially normal morphologically for about 3 days before the onset of rapid atrophy and death. Moreover, most of the neural cell death that occurs in the LGN after axotomy takes place in the last half of the first postoperative week.
成年大鼠视觉皮层（皮层区域17、18和18a）单侧受损后，同侧背外侧膝状核（LGN）中的神经元会发生轴突切断，进而导致其萎缩和死亡。对这种神经元变性的时间进程进行了定量研究，并用胶质纤维酸性蛋白免疫组织化学方法检测了星形胶质细胞的反应。在视觉皮层受损后的头3天，同侧LGN中超过95%的神经元存活。然而，在接下来的4天里，大量神经元死亡，到术后第一周结束时，存活神经元的数量减少到正常数量的约33%。在术后2周和24周之间，LGN中存在的神经元数量从正常数量的34%非常缓慢地下降到17%。视觉皮层受损3天后，同侧LGN神经元的平均横截面积比正常情况小13%（为正常的87%）。到手术后1周时，存活的LGN神经元已萎缩到其正常面积的66%。随后，存活神经元的大小在皮层损伤后24周时缓慢下降到正常大小的约50%。同侧LGN中的星形胶质细胞也会对皮层损伤做出反应。视觉皮层受损1天后，LGN中的胶质纤维酸性蛋白免疫反应几乎无法检测到，但在3天时可见免疫反应明显增加。免疫反应在术后1周和2周之间达到峰值，此后至少24周内一直很强。因此，视觉皮层受损后，LGN中神经元的胞体在快速萎缩和死亡开始前的大约3天内形态基本保持正常。此外，轴突切断后LGN中发生的大多数神经细胞死亡发生在术后第一周的后半段。
