Aims: 

Postconditioning can be induced by a broad range of stimuli within minutes to days after an ischemic insult in the brain. A special form is elicited by pharmacological intervention called second pathophysiological stress.

Methods: 

The present study aimed to evaluate the effects of low-dose (5 mg/kg) kainate postconditioning with onsets 0, 24 and 48 h after the ischemic insult on the hippocampal synaptic plasticity in a 2-vessel occlusion model in rat. The hippocampal function was tested by LTP measurements of Schaffer collateral-CA1 pyramidal cell synapses in acute slices and the changes in density of Golgi-Cox stained apical dendritic spines.

Results: 

Postconditioning 0 and 24 h after ischemia was not protective, whereas the 48-h-onset postconditioning resulted in the reappearance of a normal spine density (>100,000 spines) 3 days after ischemia, in parallel with the long-term restoration of the damaged LTP function. Similar, but somewhat less effects were observed after 10 days.

Conclusion: 

Our data clearly demonstrate the onset dependence of postconditioning elicited by a subconvulsant dose of kainate treatment in global ischemia, with restoration of the structural plasticity and hippocampal function.

Acknowledgments: 

This work was supported by TÁMOP-4.2.1/B-09/1/KONV-2010-0005, OTKA K 75628 and GVOP-3.2.1-2004-04-0357/3.0. T.F. was a Bolyai Fellow of the Hungarian Academy of Sciences.