Responses of lateral geniculate neurons that survive long-term visual cortex damage in kittens and adult cats
Responses of lateral geniculate neurons that survive long-term visual cortex damage in kittens and adult cats
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DOI：
10.1523/jneurosci.09-01-00280.1989
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发表时间：
1989-01
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影响因子：
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通讯作者：
N. Tumosa;M. McCall;W. Guido;PD Spear
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文献类型：
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作者：
N. Tumosa;M. McCall;W. Guido;PD Spear
幼猫或成年猫视皮层（17-19区）的损伤导致外侧膝状体背侧核（LGN）神经元严重退行性变性。然而，在任何年龄的视觉皮层损伤后，一些神经元存活在LGN的其他退化部分。以往的研究表明，在不同年龄的猫接受视皮层损伤后，存活的LGN细胞的潜在视网膜输入、索马大小、突触连接、输出和输出靶点的生理特性存在明确的差异。本实验研究了这些差异与存活的LGN神经元对视觉刺激的反应之间的关系。记录来自在出生当天、8周龄或成年时（存活时间为11.5-36个月）接受视觉皮层损伤的猫的LGN退化A层和C层中存活的神经元。研究了正常成年猫进行比较。绘制视觉感受野，并进行测试，将每个细胞分类为X，Y或W。此外，定量方法被用来评估响应幅度，强度的感受野环绕抑制，空间频率调谐漂移或反相正弦波光栅，并响应非优势眼刺激每个细胞。我们发现，在所有LGN层中存活的细胞对光有反应，具有正常的感受野组织，并且在任何测试年龄的病变后具有正常的眼优势。此外，LGN的大体视网膜组织是正常的。然而，在所有3个年龄段的病变后观察到2个主要异常。首先，A层中X细胞的百分比减少，从正常LGN中的62%减少到退化LGN中的约15%。第二，A层和C层的许多存活细胞具有异常大的感受野中心。在正常A层细胞和存活的A层细胞之间观察到的其他差异可能归因于X细胞的丢失。这些结果表明，在脑损伤后表现出严重退行性变性的结构内的细胞可以保持相对正常的功能，并且可以参与潜在的重要残留神经通路。以往的研究表明，这些残留的途径可以显示脑损伤的解剖和生理补偿，目前的研究结果对这种补偿的后果和机制。
Damage to visual cortex (areas 17–19) in kittens or adult cats produces severe retrograde degeneration of neurons in the dorsal lateral geniculate nucleus (LGN). However, some neurons survive in otherwise degenerated portions of the LGN after a visual cortex lesion at any age. Previous studies have shown that there are well-defined differences in potential retinal inputs, soma size, synaptic connections, outputs, and physiological properties of output targets of the surviving LGN cells in cats that received visual cortex damage at different ages. The present experiment investigated the relationships between these differences and the responses of surviving LGN neurons to visual stimulation. Recordings were made from surviving neurons in the degenerated A- and C-layers of the LGN in cats that had received a visual cortex lesion on the day of birth, at 8 weeks of age, or as adults (survival was 11.5–36 months). Normal adult cats were studied for comparison. The visual receptive field was mapped, and tests were carried out to classify each cell as X, Y, or W. In addition, quantitative methods were used to assess response amplitude, strength of receptive-field surround inhibition, spatial-frequency tuning to drifting or counterphased sine-wave gratings, and response to nondominant-eye stimulation for each cell. We found that surviving cells in all LGN layers respond to light, have normal receptive-field organization, and have normal eye dominance following a lesion at any age tested. In addition, gross retinotopic organization of the LGN is normal. However, 2 main abnormalities were observed following a lesion at all 3 ages. First, there is a reduction in the percentage of X cells in the A layers, from 62% in normal LGNs to about 15% in degenerated LGNs. Second, many surviving cells in both the A- and C-layers have abnormally large receptive-field centers. Other differences that were observed between normal A-layer cells and surviving A-layer cells could be attributed to the loss of X cells. These results indicate that cells within a structure that shows severe retrograde degeneration after brain damage can maintain relatively normal function and can take part in potentially important residual neural pathways. Previous studies indicate that these residual pathways can show both anatomical and physiological compensation for the brain damage, and the present findings bear on the consequences and mechanisms of this compensation.