Lesion of the subthalamic nucleus reverses motor deficits but not death of nigrostriatal dopaminergic neurons in a rat 6-hydroxydopamine-lesion model of Parkinson's disease

The possible role of cerium oxide (CeO2) nanoparticles in prevention of neurobehavioral and neurochemical changes in 6-hydroxydopamine-induced parkinsonian disease

“…There was reduction in the number of rears and squares crossed, and increase in latency to start moving and rearing suggesting bradykinesia. This was in agreement with Rizelio et al 35 who found impaired motor activity in 6-OHDA rat model. It has been reported that 6-OHDA lesion induced bradykinesia with the contralateral forelimb.…”

Subthalamotomy in the treatment of Parkinson's disease: clinical aspects and mechanisms of action

“…115,131,140 It was, however, shown that the phenotype, measured by tyrosine hydroxylase immunohistochemistry, the rate-limiting enzyme in the production of dopamine synthesis, was preserved in the surviving cells in the first weeks after exposure to 6-OHDA. 36,131,187 On the contrary, some authors observed neuroprotection in rats with small dopamine depletion, 133 but its effectiveness decreased in a time-dependent manner and was no longer detected after 1 week.…”

History and future challenges of the subthalamic nucleus as surgical target: Review article

“…Conversely, when tyrosine hydroxylase was measured by immunohistochemistry, the rate limiting enzyme in the production of dopamine, STN lesion, or DBS appears to provide neuroprotection to the dopaminergic nigro‐striatal pathway by normalizing glutamate release . Finally, benefits were reported in the rotatory behavior of rats treated with 6‐OHDA and subthalamic lesion, with no apparent neuroprotective effect on dopaminergic neurons . This discrepancy in the results from rodents treated with 6‐OHDA and STN lesions in terms of any possible neuroprotective response may be related to factors such as the degree of dopaminergic depletion in the striatum, the extent of STN lesion, or the time between toxin administration and subthalamotomy …”

“…Indeed, dopamine loss in the STN was an early phenomenon in asymptomatic MPTP monkeys and it was more pronounced than in the striatum . However, more variable outcomes were produced in other studies, failing to demonstrate a neuroprotective effect of prior subthalamotomy in rats treated with 6‐OHDA . Conversely, when tyrosine hydroxylase was measured by immunohistochemistry, the rate limiting enzyme in the production of dopamine, STN lesion, or DBS appears to provide neuroprotection to the dopaminergic nigro‐striatal pathway by normalizing glutamate release .…”