Electrophysiology of cerebral ischemia and reperfusion: First evidence for the role of synapse in ischemic tolerance

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The subthreshold brain-damaging stimulus may protect the brain from subsequent ischemia; this phenomenon has been named “ischemic tolerance” (IT). We focused on the synaptic properties of the neurons after mild and severe ischemia to determine the association between IT and synaptic efficacy.

Experimental design:

Adult male rats were randomly divided into four experimental groups including control, sham, permanent ischemia (pI/R), and mild ischemia (mI/R). Middle cerebral artery occlusion (MCAO) method was applied to induce brain ischemia. Seven days after the insult, long-term potentiation (LTP) induced by high-frequency stimulation (HFS) and paired-pulse ratio (PPR) were monitored before and after the HFS delivery.


The field potential recording demonstrated that mild ischemia significantly increased the basal synaptic transmission. Additionally, the HFS produced a significant potentiation compared to its baseline level in the mI/R group. Moreover, mild ischemia prevented depression of PPR by HFS. This effect was accompanied by a significant increase in the normalized PPR (PPR after HFS/PPR before HFS) in this group.


Our data indicated that a mild reduction in brain perfusion without permanent lesion can dramatically increase the basal synaptic transmission. This effect may be associated with an increase in the neurotransmitter content of the pre-synaptic neurons. This hypothesis could provide a new insight into the relationship between IT and synaptic efficacy. Synapse 70:351–360, 2016. © 2016 Wiley Periodicals, Inc.

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