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Genetic absence epilepsy rats from Strasbourg have increased corticothalamic expression of stargazin.

Authors: Powell, K L  Kyi, M  Reid, C A  Paradiso, L  D'Abaco, G M  Kaye, A H  Foote, S J  O'Brien, T J 
Citation: Powell KL, etal., Neurobiol Dis. 2008 Aug;31(2):261-5. doi: 10.1016/j.nbd.2008.04.012. Epub 2008 May 10.
Pubmed: (View Article at PubMed) PMID:18556211
DOI: Full-text: DOI:10.1016/j.nbd.2008.04.012

Stargazin is membrane bound protein involved in trafficking, synapse anchoring and biophysical modulation of AMPA receptors. A quantitative trait locus in chromosome 7 containing the stargazin gene has been identified as controlling the frequency and duration of absence seizures in the Genetic Absence Epilepsy Rats from Strasbourg (GAERS). Furthermore, mutations in this gene result in the Stargazer mouse that displays an absence epilepsy phenotype. GAERS stargazin mRNA expression is increased 1.8 fold in the somatosensory cortex and by 1.3 fold in the thalamus. The changes were present before and after the onset of absence seizures indicating that increases are not a secondary consequence of the seizures. Stargazin protein expression was also significantly increased in the somatosensory cortex after the onset of spontaneous seizures. The results are of significant importance beyond the GAERS model, as they are the first to show that an increase in stargazin expression may be pro-epileptic.


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CRRD Object Information
CRRD ID: 13524553
Created: 2018-04-19
Species: All species
Last Modified: 2018-04-19
Status: ACTIVE


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