title: Kainate postconditioning restores LTP in ischemic hippocampal CA1: onset-dependent second pathophysiological stress.
abstract: 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.
authors.affiliation: Department of Physiology, Anatomy and Neuroscience, University of Szeged, Szeged, Hungary.
authors.forename: Dávid
authors.initials: D
authors.lastname: Nagy
authors.forename: Kitti
authors.initials: K
authors.lastname: Kocsis
authors.forename: János
authors.initials: J
authors.lastname: Fuzik
authors.forename: Máté
authors.initials: M
authors.lastname: Marosi
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Kis
authors.forename: Vivian I
authors.initials: VI
authors.lastname: Teichberg
authors.forename: József
authors.initials: J
authors.lastname: Toldi
authors.forename: Tamás
authors.initials: T
authors.lastname: Farkas
mesh_terms: D000818:Animals; D056547:CA1 Region, Hippocampal / Q000187:drug effects / Q000502:physiology*; D004353:Drug Evaluation, Preclinical; D004569:Electroencephalography; D055724:Electrophysiological Phenomena / Q000187:drug effects / Q000502:physiology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D002546:Ischemic Attack, Transient / Q000401:mortality / Q000503:physiopathology; D007608:Kainic Acid / Q000494:pharmacology*; D017774:Long-Term Potentiation / Q000187:drug effects* / Q000502:physiology; D008297:Male; D058990:Molecular Targeted Therapy; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000187:drug effects / Q000502:physiology
chemical_list: D018690:Excitatory Amino Acid Agonists; D007608:Kainic Acid