Source:http://linkedlifedata.com/resource/pubmed/id/20837105
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2010-11-8
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pubmed:abstractText |
Brief, 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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1873-7544
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pubmed:author | |
pubmed:copyrightInfo |
Copyright © 2010 IBRO. Published by Elsevier Ltd. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
171
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
556-65
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pubmed:meshHeading |
pubmed-meshheading:20837105-Amygdala,
pubmed-meshheading:20837105-Animals,
pubmed-meshheading:20837105-CA3 Region, Hippocampal,
pubmed-meshheading:20837105-Cell Count,
pubmed-meshheading:20837105-Cell Death,
pubmed-meshheading:20837105-Cytoprotection,
pubmed-meshheading:20837105-Kainic Acid,
pubmed-meshheading:20837105-Male,
pubmed-meshheading:20837105-Mice,
pubmed-meshheading:20837105-Mice, Inbred C57BL,
pubmed-meshheading:20837105-Mossy Fibers, Hippocampal,
pubmed-meshheading:20837105-Neurons,
pubmed-meshheading:20837105-Neuropeptide Y,
pubmed-meshheading:20837105-Seizures,
pubmed-meshheading:20837105-Status Epilepticus,
pubmed-meshheading:20837105-Synapses,
pubmed-meshheading:20837105-Time Factors
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pubmed:year |
2010
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pubmed:articleTitle |
Epileptic 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.
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pubmed:affiliation |
Department of Physiology & Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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