Genetic absence epilepsy rats from Strasbourg have increased corticothalamic expression of stargazin
- Author(s)
- Powell, KL; Kyi, M; Reid, CA; Paradiso, L; D'Abaco, GM; Kaye, AH; Foote, SJ; O'Brien, TJ;
- Details
- Publication Year 2008-08,Volume 31,Issue #2,Page 261-265
- Journal Title
- NEUROBIOLOGY OF DISEASE
- Publication Type
- Journal Article
- Abstract
- 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. (C) 2008 Elsevier Inc. All rights reserved.
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- AMPA RECEPTOR TRAFFICKING; 3'-UNTRANSLATED REGION; CALCIUM-CHANNELS; MODEL; SEIZURES; NEURONS; LOCALIZATION; PROTEINS; SUBUNITS
- Publisher's Version
- https://doi.org/10.1016/j.nbd.2008,04.012
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2008-08-01 12:00:00