Library Open Repository
Genetic absence epilepsy rats from Strasbourg have increased corticothalamic expression of stargazin
Powell, KL and Kyi, M and Reid, CA and Paradiso, L and D'Abaco, GM and Kaye, AH and Foote, SJ and O'Brien, TJ (2008) Genetic absence epilepsy rats from Strasbourg have increased corticothalamic expression of stargazin. Neurobiology of Disease, 31 (2). pp. 261-265.
Powell_Neurobio...pdf | Request a copy
Full text restricted
Available under University of Tasmania Standard License.
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.
|Journal or Publication Title:||Neurobiology of Disease|
|Page Range:||pp. 261-265|
|Identification Number - DOI:||10.1016/j.nbd.2008.04.012|
The definitive version is available at http://www.sciencedirect.com
|Date Deposited:||21 Jul 2008 00:11|
|Last Modified:||18 Nov 2014 03:45|
|Item Statistics:||View statistics for this item|
Actions (login required)
|Item Control Page|