Dysfunctions of Ca 2+ homeostasis and of mitochondria have been studied in immortalized
striatal cells from a commonly used Huntington disease mouse model. Transcriptional
changes in the components of the phosphatidylinositol cycle and in the receptors for myo-
inositol trisphosphate-linked agonists have been found in the cells and in the striatum of the
parent Huntington disease mouse. The overall result of the changes is to delay myo-inositol
trisphosphate production and to decrease basal Ca 2+ in mutant cells. When tested directly …