Anterior thalamic lesions stop immediate early gene activation in selective laminae of the retrosplenial cortex: evidence of covert pathology in rats?
Anterior thalamic lesions stop immediate early gene activation in selective laminae of the retrosplenial cortex: evidence of covert pathology in rats?
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DOI：
10.1111/j.0953-816x.2004.03421.x
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发表时间：
2004-06-01
影响因子：
3.4
通讯作者：
Aggleton, JP
中科院分区：
文献类型：
--
作者：
Jenkins, TA;Vann, SD;Aggleton, JP
病变涉及丘脑前核停止立即早期基因（IEG）的活性在特定区域的大鼠压后皮质，即使没有明显的细胞结构的变化。离散前丘脑病变兴奋毒素（实验1）或射频（实验2），恢复后，大鼠在一个新的房间里的径向臂迷宫觅食。术后6-12周的测量表明，与手术对照相比，丘脑病变产生了相同的选择性Fos变化模式，与方法无关。颗粒（尾部颗粒皮质和喙部颗粒皮质），但不dysgranular（dysgranular皮质），压后皮质表现出Fos阳性细胞的显着损失。虽然在浅层中发现79%至89%的Fos阳性细胞丢失，但深层似乎正常。在实验3和4中，大鼠9-10个月术后被放置在一个活动箱中30分钟。前丘脑病变（实验3）导致整个压后皮质，现在包括dysgranular区的Fos和zif 268的IEG显着下降。即使使用标准组织学技术发现相同区域正常，也发现这些IEG丢失。后嗅皮层的损伤（实验4）并没有导致压后IEG活动的丧失，即使该区域也与压后皮层相连。前丘脑损伤对压后活动的这种选择性影响可能既放大了前丘脑损伤的破坏性影响，又有助于解释阿尔茨海默病中发现的后扣带回活动减退。
Lesions involving the anterior thalamic nuclei stopped immediate early gene (IEG) activity in specific regions of the rat retrosplenial cortex, even though there were no apparent cytoarchitectonic changes. Discrete anterior thalamic lesions were made either by excitotoxin (Experiment 1) or radiofrequency (Experiment 2) and, following recovery, the rats foraged in a radial-arm maze in a novel room. Measurements made 6-12 weeks postsurgery showed that, in comparison with surgical controls, the thalamic lesions produced the same, selective patterns of Fos changes irrespective of method. Granular (caudal granular cortex and rostral granular cortex), but not dysgranular (dysgranular cortex), retrosplenial cortex showed a striking loss of Fos-positive cells. While a loss of between 79 and 89% of Fos-positive cells was found in the superficial laminae, the deeper layers appeared normal. In Experiments 3 and 4, rats 9-10 months postsurgery were placed in an activity box for 30 min. Anterior thalamic lesions (Experiment 3) led to a pronounced IEG decrease of both Fos and zif268 throughout the retrosplenial cortex that now included the dysgranular area. These IEG losses were found even though the same regions appeared normal using standard histological techniques. Lesions of the postrhinal cortex (Experiment 4) did not bring about a loss of retrosplenial IEG activity even though this region is also reciprocally connected with the retrosplenial cortex. This selective effect of anterior thalamic damage upon retrosplenial activity may both amplify the disruptive effects of anterior thalamic lesions and help to explain the posterior cingulate hypoactivity found in Alzheimer's disease.