Regulatory mechanism of synaptic plasticity in the abnormally developed visual cortex

我们用Keolin注射液诱发的实验性脑积水来研究大脑皮层的功能重组。我们通过多种影像学方法证实脑室扩大和皮质层变薄，并通过脑室-腹腔分流术维持模型动物的良好状态。通过使用内在光学成像方法，我们发现在这些模型动物中，区域17和18中的取向图几乎以正常方式形成。通过在异常薄的视皮层中引入微电极，我们成功地记录了单个单位的活动，并发现一些神经元表现出正常的感受野特性。然而，它们中的大多数是单眼的，这表明这些动物的双眼视觉所需的神经元回路发育不良。体外脑片实验表明，脑积水猫视皮层神经元对注入细胞的去极化电流能产生正常的动作电位。它们的树突状结构在这些细胞中发育不良。我们进一步研究了脑积水猫的视觉皮层的代谢活动，通过使用正电子发射断层扫描。使用F18标记的脱氧葡萄糖的PET成像显示，视觉皮层的内侧库具有相对较高的示踪剂摄取活性，然而，在这些动物中，视觉皮层中的一般代谢活性明显较低。这些结果表明，在发育过程中诱导的功能重组，以补偿结构和代谢异常。

We have used experimental hydrocephalus induced by Keolin injection to study the functional reorganization of the cerebral cortex. We confirmed enlargement of cerebral ventricles and thinner cortical layers by several imaging methods and maintained model animals in good conditions by performing cerebral ventricular-peritoneal cavity shunting operation. By using an intrinsic optical imaging method, we found that the orientation maps in areas 17 and 18 were formed almost in normal manner in these model animals. By introducing a microelectrode in the abnormally thinner visual cortex, we succeeded to record single unit activities and found that some neurons showed normal receptive field properties. However, most of them were monocular, indicating the neuronal circuits required for binocular vision were poorly developed in these animals. In vitro slice experiments showed that visuocortical neurons in hydrocephalus cats could generate normal action potentials responding to the depolarizing currents injected into the cells. Their dendritic structures were poorly developed in these cells. We further examined metabolic activity of the visual cortex of hydrocephalus cats by use of positron emission tomography. PET imaging using F18-labelled deoxyglucose showed that medial bank of the visual cortex has relatively higher uptake activity of the tracer, however general metabolic activity in the visual cortex was clearly lower in these animals. These results indicate that the functional reorganization was induced during development to compensate the structural and metabolic abnormality.