School of Psychology, Cardiff University, Wales CF10 3AT, UK.
Neuroscience. 2010 Sep 1;169(3):1255-67. doi: 10.1016/j.neuroscience.2010.05.055. Epub 2010 Jun 4.
There is growing evidence that lesions of the anterior thalamic nuclei cause long-lasting intrinsic changes to retrosplenial cortex, with the potential to alter its functional properties. The present study had two goals. The first was to identify the pattern of changes in eight markers, as measured by in-situ hydridisation, in the granular retrosplenial cortex (area Rgb) following anterior thalamic lesions. The second was to use retrograde trans-neuronal tracing methods to identify the potential repercussions of intrinsic changes within granular retrosplenial cortex. In Experiment 1, adult rats received unilateral lesions of the anterior thalamic nuclei and were perfused 4 weeks later. Of the eight markers, four (c-fos, zif268, 5ht2rc, kcnab2) showed a very similar pattern of change, with decreased levels in superficial retrosplenial cortex (lamina II) in the ipsilateral hemisphere but little or no change in deeper layers (lamina V). A fifth marker (cox6b) showed a shift in activity levels in the opposite direction to the previous four markers. Three other markers (cox6a1, CD74, ncs-1) did not appear to change activity levels after surgery. The predominant pattern of change, a decrease in superficial cortical activity, points to potential alterations in plasticity and metabolism. In Experiment 2, wheat germ agglutin (WGA) was injected into the anterior thalamic nuclei in rats given different survival times, sometimes in combination with the retrograde, fluorescent tracer, Fast Blue. Dense aggregations of retrogradely labeled cells were always found in lamina VI of granular retrosplenial cortex, but additional labeled cells in lamina II were only found: (1) in WGA cases, that is never after Fast Blue injections, and (2) after longer WGA survival times (3 days). These layer II Rgb cells are likely to have been trans-neuronally labeled, revealing a pathway from lamina II of Rgb to those deeper retrosplenial cells that project directly to the anterior thalamic nuclei.
越来越多的证据表明，前丘脑核的病变会导致后穹窿皮质长期的内在变化，有可能改变其功能特性。本研究有两个目的。第一个目的是确定在接受单侧前丘脑核损伤后 4 周，通过原位杂交测量的八个标记物在后穹窿皮质颗粒层（区域 Rgb）的变化模式。第二个目的是使用逆行跨神经元追踪方法来确定颗粒后穹窿皮质内的内在变化的潜在影响。在实验 1 中，成年大鼠接受单侧前丘脑核损伤，并在 4 周后进行灌注。在这 8 个标记物中，有 4 个（c-fos、zif268、5ht2rc、kcnab2）表现出非常相似的变化模式，同侧半球浅层后穹窿皮质（层 II）的水平降低，但深层（层 V）的变化很小或没有。第 5 个标记物（cox6b）显示出与前 4 个标记物相反的活性水平变化。另外 3 个标记物（cox6a1、CD74、ncs-1）在手术后似乎没有改变活性水平。主要的变化模式是浅层皮质活性的降低，这表明潜在的可塑性和代谢变化。在实验 2 中，在给予不同存活时间的大鼠的前丘脑核中注射了麦胚凝集素（WGA），有时与逆行、荧光示踪剂 Fast Blue 联合使用。在颗粒后穹窿皮质的层 VI 中总是发现密集的逆行标记细胞聚集，但仅在以下情况下才发现层 II 中的额外标记细胞：（1）在 WGA 情况下，即从未在 Fast Blue 注射后发现，以及（2）在更长的 WGA 存活时间（3 天）后。这些层 II Rgb 细胞很可能是通过跨神经元标记的，揭示了从 Rgb 的层 II 到那些直接投射到前丘脑核的更深层后穹窿细胞的途径。
