Henrich-Noack Petra, Gorkin Alexander G, Reymann Klaus G
Leibniz Institute for Neurobiology, Brenneckestreet 6, 39118, Magdeburg, Germany.
Exp Brain Res. 2007 Jul;181(1):79-86. doi: 10.1007/s00221-007-0907-2. Epub 2007 Mar 13.
Recordings of the electroencephalogram (EEG) are regularly used to asses the severity of transient global ischaemia in rats. Here, we investigated whether the EEG obtained from electrodes placed in the hippocampus does indeed give valuable information about the consequences of an ischaemic event. Furthermore, we evaluated how evoked synaptic responses from the same electrodes placed in the hippocampal CA1 area changed with time and in relation to damage. We performed transient two vessel-occlusion with hypobaric hypotension in rats to induce selective, delayed neuronal death in CA1. Beforehand, the animals had been chronically implanted with electrodes. Stimulating electrodes had been placed into the Schaffer collaterals and recording electrodes into the CA1 area. EEG was recorded from shortly before ischaemia until up to 40 min post-ischaemia. Field excitatory post-synaptic potentials (fEPSP) were recorded before ischaemia or sham-operation and 2 and 7 days afterwards. We found a significant negative correlation between the duration of the EEG amplitude decrease (flattening) and the number of surviving neurons in CA1, which were quantified by histology after 7 days post-ischaemia. However, substantial neuronal damage was only seen when the time of flattening was more than 12 min and outlasted the time of ischaemia. The impairment of synaptic function, measured as the decrease of fEPSP slope 2 days post-ischaemia correlated with the later maturated structural damage in CA1. The fEPSP remained decreased until day 7 post-ischaemia. Animals with no damage (sham condition) showed a transient decrease of the fEPSP slope. In conclusion, our data show that the duration of EEG-flattening predicts the extent of neuronal damage. However, EEG-flattening just during the period of clamping both common carotid arteries--albeit an essential precondition for substantial CA1 cell loss to occur--is not sufficient to predict damage. The degree of impairment of evoked synaptic function of CA1 neurons (fEPSP) 2 days after ischaemia predicts the final extent of damage with significant probability.
脑电图(EEG)记录常被用于评估大鼠短暂性全脑缺血的严重程度。在此,我们研究了从置于海马体的电极获取的脑电图是否确实能提供有关缺血事件后果的有价值信息。此外,我们评估了置于海马体CA1区的相同电极诱发的突触反应如何随时间变化以及与损伤的关系。我们对大鼠进行了伴有低压性低血压的短暂双血管闭塞,以诱导CA1区选择性、延迟性神经元死亡。在此之前,动物已被长期植入电极。刺激电极置于沙费尔侧支,记录电极置于CA1区。从缺血前不久直至缺血后40分钟记录脑电图。在缺血或假手术前以及之后2天和7天记录场兴奋性突触后电位(fEPSP)。我们发现脑电图幅度下降(平坦化)的持续时间与CA1区存活神经元数量之间存在显著负相关,缺血后7天通过组织学对存活神经元数量进行了量化。然而,只有当平坦化时间超过12分钟且持续时间超过缺血时间时,才会出现大量神经元损伤。以缺血后2天fEPSP斜率下降来衡量的突触功能损害与CA1区后期成熟的结构损伤相关。fEPSP在缺血后第7天之前一直降低。无损伤(假手术情况)的动物fEPSP斜率出现短暂下降。总之,我们的数据表明脑电图平坦化的持续时间可预测神经元损伤的程度。然而,仅在夹闭双侧颈总动脉期间出现的脑电图平坦化——尽管这是发生大量CA1细胞丢失的必要前提条件——不足以预测损伤。缺血后2天CA1神经元诱发突触功能的损害程度(fEPSP)有很大概率可预测最终的损伤程度。