Protein kinase C beta II mRNA levels decrease in the striatum and cortex of transgenic Huntington's disease mice

Huntington's disease (HD) is caused by the inheritance of the huntingtin ge ne with an expanded CAG; repeat. The function of the normal or mutant form of the huntingtin protein remains to be determined. We used differential di splay to determine differences in steady-state mRNA levels between wild-typ e and the R6/2 transgenic mouse model of HD. Using this method, we determin ed that the steady-state mRNA levels of protein kinase C beta II (PKC beta II) subunit are decreased in symptomatic HD mice compared with age-matched wild-type controls. The decrease in PKC beta II mRNA levels occurred in bot h the striatum and cortex. Previously, it had been demonstrated that PKC be ta II immunoreactivity is decreased in the caudate-putamen of patients with Huntington's disease. PKC has been implicated in the long-term potentiatio n model of brain plasticity and learning, and the loss of PKC may affect in formation storage in HD. The expression of htt-HD throughout the brain affe cts the transcription of specific genes in regions not associated with wide spread neurodegeneration.