ArticleExperimental brain research2007
Predictive value of changes in electroencephalogram and excitatory postsynaptic field potential for CA1 damage after global ischaemia in rats.
Article in Experimental brain research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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3 authors at 2 institutions in 2 countries.
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Abstract
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.
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