Kainate postconditioning restores LTP in ischemic hippocampal CA1 Onset-dependent second pathophysiological stress /
Postconditioning can be induced by a broad range of stimuli within minutes to days after an ischemic cerebral insult. A special form is elicited by pharmacological intervention called second pathophysiological stress. The present study aimed to evaluate the effects of low-dose (5 mg/kg) kainate post...
Elmentve itt :
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| Dokumentumtípus: | Cikk |
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Pergamon Press
2011
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| Sorozat: | NEUROPHARMACOLOGY
61 No. 5-6 |
| doi: | 10.1016/j.neuropharm.2011.07.005 |
| mtmt: | 1746145 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/8850 |
| Tartalmi kivonat: | Postconditioning can be induced by a broad range of stimuli within minutes to days after an ischemic cerebral insult. A special form is elicited by pharmacological intervention called second pathophysiological stress. 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. Postconditioning 0 and 24 h after ischemia was not protective, whereas 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. 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. © 2011 Elsevier Ltd. All rights reserved. |
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| Terjedelem/Fizikai jellemzők: | 1026-1032 |
| ISSN: | 0028-3908 |