Abstract
The relationship between the specific neuronal loss observed in Huntington's disease and the mutation in the IT15 gene responsible for this disease remains obscure. Using an antipeptide antibody against amino acids 3114-3141 of the human huntingtin protein, we demonstrate that striatal injection of quinolinic acid in mice induces increased immunoreactivity for huntingtin in some remaining neurons but not in glial cells. This increase is apparent in both neuronal cell bodies and in cell processes in the white matter six hours after excitotoxic challenge. This finding suggests that huntingtin may be involved in the response to excitotoxic stress in these neurons.
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