本實驗以高嶺土誘發大鼠產生阻塞型水腦症,探討手術後一週(急性期)和八週(慢性期)大鼠感覺運動皮質所受的影響。阻塞型水腦明顯降低了大鼠體重的增加速率。大鼠的顱內壓在急性期上升將近3倍,而在慢性期則降低至1.8倍。不管是急性期或慢性期,大鼠的大腦皮質層厚度明顯減少,但皮質中神經元的密度並沒有明顯改變。在急性期同時會引起星形神經膠細胞的活化,而小膠細胞則無明顯變化。此外,皮質中高度表現一氧化氮合成酶的神經細胞數目在正常皮質中的密度不高,在急性期稍微減少,但在慢性期皮質中的密度則與正常組相當。為探討皮質的功能是否會因水腦而改變,我們以細胞內染料注射法研究探討感覺運動皮質第五層錐狀神經元整體樹突叢的變化,結果顯示,在急性期神經元樹突總長度,尤其是頂樹突的長度會明顯減少,至於樹突棘的密度則在急性期和慢性期都明顯減少。綜合上述,我們的結果顯示急性阻塞型水腦症會造成感覺運動皮質變薄,同時改變第五層錐狀神經元的樹突叢,而這種變化會持續到慢性期。而水腦症造成對第五層錐狀神經元樹突棘密度的降低則可能代表感覺運動皮質接受訊息的功能,間接的輸出的功能明顯受到了影響。
The effects of obstructive hydrocephalus on cerebral cortex was studied on rats with kaolin-induced hydrocephalus. The sensorimotor cortex was studied 1 (acute) and 8 weeks (chronic) following kaolin injection. Obstructive hydrocephalus slowed the weight gain of rats significantly. The intracranial pressures of animals increased to close to 3 folds in acute and drop to 1.8 fold of control levels in chronic cases. The thickness of the Cortex of both acute and chronic animals were all significantly reduced, however with no apparent neuronal loss. Reactive changes of astrocytes, but not microglia, were observed in acute cases. The density of the intensively NOS-positive neurons in normal cortex was low and decreased slightly in acute cases but returned to normal level in chronic cortices. Intracellular dye injection revealed that the length of the dendrites, especially the apical dendrites of layer Ⅴ pyramidal neurons of the acute hydrocephalic animals was significantly decreased. The densities of dendritic spines on the layer Ⅴ pyramidal neurons of both acute and chronic animals were significantly decreased. In conclusion, our results show that obstructive hydrocephalus caused a fast onset of the thinning of the sensorimotor cortex and the remodeling of the dendritic arbors of layer V pyramidal neurons and these phenomena persisted in chronic animals. The reduction of the dendritic spines of layer V pyramidal neurons suggest that the input, and consequently output of the sensorimotor cortices of the hydrocephalic animals were compromised.