Source:http://linkedlifedata.com/resource/pubmed/id/15053958
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1-2
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pubmed:dateCreated |
2004-3-31
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pubmed:abstractText |
Due to the involvement of cortical neurons in spike-wave discharge (SWD) initiation, and the contribution of voltage-gated sodium channels (VGSCs) to neuronal firing, we examined alterations in the expression of VGSC mRNA and protein in cortical neurons in the WAG/Rij absence epileptic rat. WAG/Rij rats were compared to age-matched Wistar control rats at 2, 4, and 6 months. Continuous EEG data was recorded, and percent time in SWD was determined. Tissue from different cortical locations from WAG/Rij and Wistar rats was analyzed for VGSC mRNA (by quantitative PCR) and protein (by immunocytochemistry). SWDs increased with age in WAG/Rij rats. mRNA levels for sodium channels Nav1.1 and Nav1.6, but not Nav1.2, were found to be up-regulated selectively within the facial somatosensory cortex (at AP +0.0, ML +6.0 mm). Protein levels for Nav1.1 and Nav1.6 were up-regulated in layer II-IV cortical neurons in this region of cortex. No significant changes were seen in adjacent regions or other brain areas, including the pre-frontal and occipital cortex. In the WAG/Rij model of absence epilepsy, we identified a specific region of cortex, in layer II-IV neurons on the lateral convexity of the cortex in the facial somatosensory area, where mRNA and protein expression of sodium channel genes Nav1.1 and Nav1.6 are up-regulated. This region of cortex approximately matches the electrophysiologically determined region of seizure onset. Changes in the expression of Nav1.1 and Nav1.6 parallel age-dependent increases in seizure frequency and duration.
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pubmed:grant | |
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 |
Mar
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pubmed:issn |
0006-8993
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
12
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pubmed:volume |
1000
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
102-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:15053958-Action Potentials,
pubmed-meshheading:15053958-Aging,
pubmed-meshheading:15053958-Animals,
pubmed-meshheading:15053958-Cerebral Cortex,
pubmed-meshheading:15053958-Disease Models, Animal,
pubmed-meshheading:15053958-Epilepsy, Absence,
pubmed-meshheading:15053958-Nerve Tissue Proteins,
pubmed-meshheading:15053958-Neurons,
pubmed-meshheading:15053958-RNA, Messenger,
pubmed-meshheading:15053958-Rats,
pubmed-meshheading:15053958-Rats, Wistar,
pubmed-meshheading:15053958-Sodium Channels,
pubmed-meshheading:15053958-Up-Regulation
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pubmed:year |
2004
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pubmed:articleTitle |
Dysregulation of sodium channel expression in cortical neurons in a rodent model of absence epilepsy.
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pubmed:affiliation |
Department of Neurology, Yale University School of Medicine, New Haven, and Rehabilitation Research Center, VA Connecticut Healthcare System, West Haven, CT, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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