Guido W, Spear P D, Tong L
Department of Psychology, University of Wisconsin, Madison 53706.
Exp Brain Res. 1992;91(3):455-66. doi: 10.1007/BF00227841.
Previous studies indicate that neurons in the cat's posteromedial lateral suprasylvian (PMLS) visual area of cortex show physiological compensation after neonatal but not adult damage to areas 17, 18, and 19 of the visual cortex (collectively, VC). Thus, VC damage in adults produces a loss of direction selectivity and a decrease in response to the ipsilateral eye among PMLS cells, but these changes are not seen in adult cats that received VC damage as kittens. This represents compensation for early VC damage in the sense that PMLS neurons develop properties they would have had if there had been no brain damage. However, this is only a partial compensation for the effects of VC damage. A full compensation would involve development of properties of the VC cells that were removed in the damage. The present study investigated whether this type of compensation occurs for detailed spatial- and temporal-frequency processing. Single-cell recordings were made in PMLS cortex of adult cats that had received a VC lesion on the day of birth or at 8 weeks of age. Responses to sine-wave gratings that varied in spatial frequency, contrast, and temporal frequency were assessed quantitatively. We found that the spatial- and temporal-frequency processing of PMLS cells in adult cats that had neonatal VC damage were not significantly different from PMLS cells in normal cats. Therefore, there was no evidence that PMLS cells can compensate for VC damage by developing properties that are better than normal and like those of the striate cortex cells that were damaged. We also assessed the effects of long-term VC damage in adult cats to determine whether the normal properties seen in cats with neonatal VC damage represent a compensation for abnormalities in PMLS cortex present after adult damage. In a previous study, we found that acute VC damage in adult cats has small but reliable effects on maximal response amplitude, maximal contrast sensitivity, and spatial resolution (Guido et al. 1990b). In the present study, we found that long-term VC damage in adult cats does not increase these abnormalities as a result of secondary degenerative changes. In fact, the minor abnormalities that were present after an acute VC lesion were virtually absent following a long-term adult lesion, perhaps because they were due to transient traumatic effects. Therefore, there was little evidence for abnormalities in spatial- or temporal-frequency processing following long-term adult VC damage for which PMLS cells might show compensation following long-term neonatal damage.(ABSTRACT TRUNCATED AT 400 WORDS)
先前的研究表明，猫视觉皮层后内侧外侧上薛氏回（PMLS）区域的神经元在视觉皮层17、18和19区（统称为VC）新生儿期而非成年期受损后会出现生理补偿。因此，成年猫的VC损伤会导致PMLS细胞方向选择性丧失以及对同侧眼反应的降低，但这些变化在幼年时接受VC损伤的成年猫中并未出现。从PMLS神经元发展出若未发生脑损伤本应具有的特性这一意义上来说，这代表了对早期VC损伤的补偿。然而，这只是对VC损伤影响的部分补偿。完全补偿将涉及发展出在损伤中被去除的VC细胞的特性。本研究调查了这种类型的补偿是否发生在详细的空间和时间频率处理中。对出生当天或8周龄时接受VC损伤的成年猫的PMLS皮层进行单细胞记录。定量评估对空间频率、对比度和时间频率变化的正弦波光栅的反应。我们发现，新生儿期VC损伤的成年猫中PMLS细胞的空间和时间频率处理与正常猫的PMLS细胞没有显著差异。因此，没有证据表明PMLS细胞可以通过发展出比正常情况更好且类似于受损纹状皮层细胞的特性来补偿VC损伤。我们还评估了成年猫长期VC损伤的影响，以确定新生儿期VC损伤的猫中所见的正常特性是否代表对成年期损伤后PMLS皮层异常的补偿。在先前的一项研究中，我们发现成年猫急性VC损伤对最大反应幅度、最大对比度敏感性和空间分辨率有微小但可靠的影响（Guido等人，1990b）。在本研究中，我们发现成年猫长期VC损伤不会因继发性退行性变化而增加这些异常。事实上，急性VC损伤后出现的微小异常在长期成年损伤后几乎不存在，可能是因为它们是由短暂的创伤效应引起的。因此，几乎没有证据表明成年猫长期VC损伤后在空间或时间频率处理方面存在异常，而PMLS细胞在长期新生儿损伤后可能会对此进行补偿。（摘要截断于400字）
