If you measured DA and its metabolites by HPLC Elecrochemical detector and believe that DOPAC amount is more in 6-OHDA lesioned striatum then the possible reason could be that the tissue was kept for a long time at Room Temperature or ice. DA gets converted to DOPAc my the mitochondrial enzyme Monoamine oxidase B to DOPAC and H2O2. If you dont deproteinize it soon the enzyme is still active and converts the residual DA to DOPAC.
Remaining DA neurons are compensating for the lesion, thus the higher DOPAC/DA ratio (which is the more informative neurochemical expression related to DA function) See RH Roth et al for DOPAC cred and Mike Zigmond et al for DOPAC/DA cred after lesion. DA levels in this experiment show the extent of lesion, i.e. the extent of DA neuronal loss. DOPAC/DA reflects ongoing neuronal activity.
Thanks for your answers. However, whether the higher levels of DOPAC are explained, why there is no HVA? Isn't HVA a direct product of DOPAC? Therefore should be more related to DOPAC levels and not DA itself...