Tsubokawa T, Katayama Y, Kawamata T
Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan.
Brain Inj. 1988 Jan-Mar;2(1):19-30. doi: 10.3109/02699058809150929.
Schaffer collateral responses recorded from CA1 pyramidal cell layers in the hippocampus were analysed in kaolin-induced hydrocephalic rats. Other features of this rat model of chronic hydrocephalus were evaluated from measurements of the intracranial pressure, Na-fluorescein migration from the ventricle to the cerebral parenchyma, and behavioural changes. The results indicated that: (1) the conduction velocity of the Schaffer collaterals was unchanged; (2) the threshold to elicit population spikes was decreased; (3) the paired-pulse facilitation of EPSP tended to increase; (4) the paired-pulse inhibition of population spikes was unchanged; and (5) the long-term potentiation of population spikes was clearly attenuated in the hydrocephalic rats. The changes seen in the long-term potentiation were less pronounced in rats which underwent kaolin injection but did not develop hydrocephalus. The above findings suggest that disturbance in the postsynaptic integration processes, rather than axonal conduction or synaptic transmission, are more important for the production of the neurological deficits seen in chronic hydrocephalus. Electron microscopic observations supporting this inference are also briefly described.
对高岭土诱导的脑积水大鼠海马CA1锥体细胞层记录的Schaffer侧支反应进行了分析。通过测量颅内压、荧光素钠从脑室向脑实质的迁移以及行为变化，评估了这种慢性脑积水大鼠模型的其他特征。结果表明：（1）Schaffer侧支的传导速度未改变；（2）引发群体峰电位的阈值降低；（3）EPSP的双脉冲易化倾向于增加；（4）群体峰电位的双脉冲抑制未改变；（5）在脑积水大鼠中，群体峰电位的长时程增强明显减弱。在接受高岭土注射但未发生脑积水的大鼠中，长时程增强的变化不太明显。上述发现表明，突触后整合过程的紊乱，而非轴突传导或突触传递，对于慢性脑积水中出现的神经功能缺损的产生更为重要。还简要描述了支持这一推论的电子显微镜观察结果。
