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Cited by (33)
Current Status, Gaps, and Weaknesses of the Mechanism of Selective Dopaminergic Toxicity of MPTP/MPP<sup>+</sup>
2017, Advances in Molecular ToxicologyCitation Excerpt :The physiological significance of these differences is not clearly understood. As mentioned above, numerous previous studies suggest that the active accumulation of MPP+ in dopaminergic synaptic vesicles through VMAT2 protects the dopaminergic cells from MPP+ toxicity [100,102–105]. This proposal is based on the argument that the synaptic accumulation limits the availability of cytosolic MPP+ for mitochondrial entry and complex I inhibition which are vital for the proposed mechanism of the neurotoxicity of MPP+.
Apparent opposite effects of tetrabenazine and reserpine on the toxic effects of 1-methyl-4-phenylpyridinium or 6-hydroxydopamine on nigro-striatal dopaminergic neurons
2003, Brain ResearchCitation Excerpt :Surprisingly, we observed that TBZ treatment (30 mg/kg, s.c.) performed 90 min before injecting 6-OHDA or MPP+, protected from both toxins. Reinhard Jr. et al. [31] have observed that a treatment with TBZ, 30 min before MPTP i.p. injection, potentiates the neurotoxicity undergone by mice. The discrepancy between the results of Naudin et al. [28], Reinhard Jr. et al. [31] and ours, may be explained by the time course of the TBZ side effects, such as hypothermia, and that a delay of 30 min between administration of TBZ and the toxin is insufficient to obtain a marked inhibition of the VMAT2.
L-DOPA does not cause neurotoxicity in VMAT2 heterozygote knockout mice
2002, NeuroToxicologyMethamphetamine neurotoxicity: Necrotic and apoptotic mechanisms and relevance to human abuse and treatment
2001, Brain Research Reviews