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首页> 外文期刊>The European Journal of Neuroscience >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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Anterior thalamic lesions stop immediate early gene activation in selective laminae of the retrosplenial cortex: evidence of covert pathology in rats?

机译：丘脑前部病变阻止了脾后皮质的选择性层中的立即早期基因激活：大鼠隐匿性病理的证据？

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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.
机译：即使没有明显的细胞结构改变，涉及前丘脑核的病变在大鼠脾后皮质的特定区域也停止了早期早期基因（IEG）活性。通过兴奋性毒素（实验1）或射频（实验2）造成丘脑前部离散病变，恢复后，大鼠在新颖房间的radial臂迷宫中觅食。术后6-12周进行的测量表明，与手术对照组相比，无论采用何种方法，丘脑病变都会产生相同的选择性Fos改变模式。颗粒状（尾状颗粒皮层和延髓颗粒状皮层），但非运动异常性（dysgranular皮质），脾后皮质则显示出明显的Fos阳性细胞丢失。尽管在浅层中发现了79％至89％的Fos阳性细胞丢失，但较深的层似乎正常。在实验3和4中，将术后9-10个月的大鼠放在活动箱中30分钟。丘脑前部病变（实验3）导致整个脾后皮质（现在包括后突区域）的Fos和zif268的IEG明显降低。即使使用标准组织学技术，即使同一区域看起来正常，也发现了这些IEG丢失。鼻后皮质的病变（实验4）并没有导致后脾IEG活性的降低，即使该区域也与后脾皮质相互联系。丘脑前部损伤对脾后活动的选择性作用可能会放大丘脑前部病变的破坏作用，并有助于解释阿尔茨海默氏病中的扣带后部功能减退。

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