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

K. L. Powell, M. Kyi, C. A. Reid, L. Paradiso, G. M. D'Abaco, A. H. Kaye, S. J. Foote, T. J. O'Brien

Research output: Contribution to journalArticleResearchpeer-review

14 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)261-265
Number of pages5
JournalNeurobiology of Disease
Issue number2
Publication statusPublished - Aug 2008


  • Absence epilepsy
  • AMPA receptors
  • Animal models
  • Somatosensory cortex
  • Stargazin
  • Thalamus

Cite this