EFFECTS OF STRIATAL EXCITOTOXICITY ON HUNTINGTON-LIKE IMMUNOREACTIVITY

THE relationship between the specific neuronal loss observed in Huntin gton's disease and the mutation in the IT15 gene responsible for this disease remains obscure. Using an antipeptide antibody against amino a cids 3114-3141 of the human huntingtin protein, we demonstrate that st riatal injection of quinolinic acid in mice induces increased immunore activity for huntingtin in some remaining neurons but not in glial cel ls. 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.