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pubmed-article:20837105pubmed:abstractTextBrief, non-harmful seizures can activate endogenous protective programmes which render the brain resistant to damage caused by prolonged seizure episodes. Whether protection in epileptic tolerance is long-lasting or influences the subsequent development of epilepsy is uncertain. Presently, we investigated the relationship between hippocampal pathology, neuropeptide Y rearrangement and spontaneous seizures in sham- and seizure-preconditioned mice after status epilepticus induced by intra-amygdala kainate. Seizure-induced neuronal death at 24 h was significantly reduced in the ipsilateral hippocampal CA3 and hilus of tolerance mice compared to sham-preconditioned animals subject to status epilepticus. Damage to the CA3-hilus remained reduced in tolerance mice 21 days post-status. In sham-preconditioned mice subject to status epilepticus correlative statistics showed there was a strong inverse relationship between CA3, but not hilar, neuron counts and the number of spontaneous seizures. A strong positive association was also found between neuropeptide Y score and spontaneous seizure count in these mice. In contrast, there was no significant association between spontaneous seizure count and CA3 neuron loss or neuropeptide Y rearrangement in the tolerance mice. These data show that tolerance-conferred neuroprotection is long-lasting and that tolerance disrupts the normal association between CA3 damage, synaptic rearrangement and occurrence of spontaneous seizures in this model.lld:pubmed
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pubmed-article:20837105pubmed:authorpubmed-author:ConroyR MRMlld:pubmed
pubmed-article:20837105pubmed:authorpubmed-author:HenshallD CDClld:pubmed
pubmed-article:20837105pubmed:authorpubmed-author:MouriGGlld:pubmed
pubmed-article:20837105pubmed:authorpubmed-author:Jimenez-Mateo...lld:pubmed
pubmed-article:20837105pubmed:copyrightInfoCopyright © 2010 IBRO. Published by Elsevier Ltd. All rights reserved.lld:pubmed
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pubmed-article:20837105pubmed:articleTitleEpileptic tolerance is associated with enduring neuroprotection and uncoupling of the relationship between CA3 damage, neuropeptide Y rearrangement and spontaneous seizures following intra-amygdala kainic acid-induced status epilepticus in mice.lld:pubmed
pubmed-article:20837105pubmed:affiliationDepartment of Physiology & Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland.lld:pubmed
pubmed-article:20837105pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:20837105pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed