Kainate postconditioning restores LTP in ischemic hippocampal CA1: Onset-dependent second pathophysiological stress

NEUROPHARMACOLOGY

卷:61

Article

Nagy, David¹  Kocsis, Kitti¹  Fuzik, Janos¹  Marosi, Mate¹  Kis, Zsolt¹  Teichberg, Vivian I.²  Toldi, Jozsef¹  Farkas, Tamas¹ 

[1] Univ Szeged, Dept Physiol Anat & Neurosci, H-6726 Szeged, Hungary

[2] Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel

关键词: 2-vessel occlusion;    CA1;    Kainic acid;    LTP;    Postconditioning;    Spine density;   

DOI  :  10.1016/j.neuropharm.2011.07.005

来源: Elsevier

【 摘 要 】

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 LIP 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 LIP 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. (C) 2011 Elsevier Ltd. All rights reserved.

【 授权许可】

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