Genetic absence epilepsy rats from Strasbourg have increased corticothalamic expression of stargazin |
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| 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 |
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| Affiliation: | aDepartment of Medicine (RMH/WH), University of Melbourne, Melbourne, Australia;bHoward Florey Institute, University of Melbourne, Melbourne, Australia;cDepartment of Surgery (RMH/WH), University of Melbourne, Melbourne, Australia;dThe Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia;eThe Menzies Research Institute, Hobart, Tasmania, Australia |
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| 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. |
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| Keywords: | Stargazin Absence epilepsy Animal models GAERS AMPA receptors Somatosensory cortex Thalamus |
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