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Overview
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Background
6-Hydroxydopamine hydrobromide (6-OHDA hydrobromide) is a catecholaminergic neurotoxin that has been used to induce dopaminergic lesions and parkinsonian symptoms as a model of Parkinson's disease in rodents[1].
6-OHDA hydrobromide (75 μM) activates caspase-3, -8, and -9 in a time-dependent manner and increases the level of intracellular reactive oxygen species (ROS) in PC12 cells and induces apoptosis in rat substantia nigra when stereotaxically injected into the right MFB[2].
6-OHDA hydrobromide induces locomotor impairment in mice and loss of tyrosine hydroxylase-reactive neurons in mouse brain when administered into the substantia nigra, medial forebrain bundle (MFB), or striatum at doses of 9, 6, and 18 μg, respectively[3].[1]. Blum D, Torch S, Lambeng N, et al. Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: Contribution to the apoptotic theory in Parkinson’s disease. Prog. Neurobiol, 2001, 65(2): 135-172.
[2]. Fujita H, Ogino T, Kobuchi H, et al. Cell-permeable cAMP analog suppresses 6-hydroxydopamine-induced apoptosis in PC12 cells through the activation of the Akt pathway. Brain Res, 2006, 1113(1): 10-23.
[3]. Heuer A, Smith G A, Lelos M J, et al. Unilateral nigrostriatal 6-hydroxydopamine lesions in mice I: Motor impairments identify extent of dopamine depletion at three different lesion sites. Behav. Brain Res, 2012, 228(1): 30-43.
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Overview