Lesions of nonvisual inputs affect plasticity, norepinephrine content, and acetylcholine content of visual cortex.
Lesions of nonvisual inputs affect plasticity, norepinephrine content, and acetylcholine content of visual cortex.
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非视觉输入的损伤会影响视觉皮层的可塑性、去甲肾上腺素含量和乙酰胆碱含量。
DOI：
10.1152/jn.1990.64.6.1851
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发表时间：
1990
影响因子：
2.5
通讯作者：
Turk,F
中科院分区：
文献类型：
--
作者：
Gordon,B;Mitchell,B;Mohtadi,K;Roth,E;Tseng,Y;Turk,F
1.视皮层中去甲肾上腺素（NE）和乙酰胆碱（ACh）的耗竭可降低可塑性。这种可塑性的下降，虽然在某些情况下是戏剧性的，但在其他情况下不会发生。2.我们在35- 42日龄幼猫的扣带回后面的白色物质上做了一个损伤，以耗尽皮质NE和ACh。一只眼睛在病变当天缝合。我们在7天或2-3个月后记录了视觉皮层，并使用剥夺眼对皮层细胞的影响作为可塑性的测量。3.我们测量NE含量的高压液相色谱法（HPLC）和推断乙酰胆碱消耗消耗胆碱乙酰转移酶（ChAT）的活性。NE耗竭成功的动物平均耗竭60%。ChAT活性的消耗与NE消耗一致。4.当记录发生7天后的病变和缝合的眼睛是对侧的病变，可塑性下降的一面与病变，70%的细胞被剥夺的眼睛驱动。在对照侧，只有15%的细胞由剥夺眼驱动。5.在两种情况下，损伤并没有导致可塑性下降。在病变同侧缝合的动物中，皮质保持可塑性。在这些动物中，只有26%的大脑半球的细胞受到剥夺眼睛的驱动。如果对侧眼在损伤后缝合数月，皮质也保持其可塑性，即使NE和ACh耗尽没有恢复。6.我们的结论是NE和ACh的耗竭确实会降低可塑性，也就是说，它可以保护被剥夺的眼睛免于失去驱动皮质细胞的能力，至少在短时间内是这样。耗竭只保护正常占优势的对侧通路;同侧视觉通路保持可塑性。7.也许剥夺眼的一侧的重要性可以通过假设NE和ACh的消耗消除易化输入来解释。这将降低损伤侧皮层细胞增强非剥夺眼相对于剥夺眼的输入的能力;也就是说，它将降低分子剥夺（MD）效应。去除易化也会增加驱动细胞所需的视觉输入。（400字处截断摘要）
1. The depletion of both norepinephrine (NE) and acetylcholine (ACh) in the visual cortex can decrease plasticity. This decrease in plasticity, although dramatic under some circumstances, fails to occur under others. 2. We depleted cortical NE and ACh in 35- to 42-day-old kittens by making a lesion of the white matter behind the cingulate gyrus. One eye was sutured on the day of the lesion. We recorded from the visual cortex 7 days or 2-3 mo later and used the influence of the deprived eye on the cortical cells as a measure of plasticity. 3. We measured NE content by high-pressure liquid chromatography (HPLC) and inferred ACh depletion from depletion of choline acetyltransferase (ChAT) activity. NE depletion averaged 60% in the successfully depleted animals. Depletion of ChAT activity was consistent with NE depletion. 4. When recording occurred 7 days after the lesion and the sutured eye was contralateral to the lesion, plasticity was decreased on the side with the lesion; 70% of the cells were driven by the deprived eye. On the control, uninjured side only 15% of the cells were driven by the deprived eye. 5. In two circumstances the lesion did not cause a decrease in plasticity. In animals with suture ipsilateral to the lesion, the cortex remained plastic. In these animals only 26% of the cells in the hemisphere with the lesion were driven by the deprived eye. The cortex also retained its plasticity if the contralateral eye remained sutured for several months after the lesion, even though there was no recovery from NE and ACh depletion. 6. We conclude that depletion of NE and ACh does decrease plasticity; that is, it protects the deprived eye from losing its ability to drive cortical cells, at least for a short period of time. Depletion protects only the normally dominant contralateral pathway; the ipsilateral visual pathway remains plastic. 7. Perhaps the importance of the side of the deprived eye can be explained by assuming that depletion of NE and ACh removes facilitatory input. This would decrease the ability of cortical cells on the side with lesion to potentiate the input from the nondeprived eye relative to the deprived eye; that is, it would decrease the molecular deprivation (MD) effect. A removal of facilitation would also increase the visual input required to drive cells.(ABSTRACT TRUNCATED AT 400 WORDS)