Abstract
The goals of this short review are to familiarize readers with the stargazer mouse and to outline the major functional defects associated with this mutant. The roles of the stargazin protein in calcium channel function and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor trafficking are discussed; focus is placed on studies regarding the thalamus, whence absence seizures potentially originate, and the cerebellum, which is associated with the ataxic phenotype. Finally, two additional alleles of stargazer, waggler and stargazer 3Jackson (3J), illustrate the value of an allelic series for understanding stargazin function.
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