Abstract
For future investigation of possible perturbation of circadian rhythm in animal models of Parkinson's disease we needed an animal model providing lasting 80-100% striatal dopaminergic depletion in rats, but without induced mortality. We have thus compared the effects of a single hydroxydopamine bilateral striatal lesion (SB-hydroxydopamine) with those of a double hydroxydopamine bilateral lesion (DB-hydroxydopamine) at the same dose (16 microg/striatum) by HPLC determination of dopamine and 3,4-dihydrophenylacetic acid (dopac) levels in the striatum. Two weeks after neurosurgery, SB-hydroxydopamine and DB-hydroxydopamine induced dopaminergic depletion of at least 81% compared with control groups. After eight weeks striatal dopaminergic depletion was only 60.97% in SB-hydroxydopamine rats, suggesting a compensatory phenomenon, whereas in DB-hydroxydopamine rats dopaminergic loss was stable at 88%. For the DB-hydroxydopamine group the dopac/dopamine ratio was significantly increased at week 2 only, whereas no significant change was observed for other groups. This increase might be explained by increased dopamine turnover. We have demonstrated that striatal DB-hydroxydopamine injection induces lasting 80-100% neuronal loss, close to that observed in the disease in man, without induced mortality, and provides a tool which meets our experimental requirements.
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