6-Hydroxydopamine hydrobromide
Chemical Name: 5-(2-Aminoethyl)-1,2,4-benzenetriol hydrobromide
Biological Activity
Selective catecholaminergic neurotoxin. Depletes brain catecholamine levels via uptake and accumulation by a transport mechanism specific to these neurons. Causes almost complete destruction of nigral dopaminergic neurons and their striatal terminals when injected into the substantia nigra of rats, producing an animal model of Parkinson's disease.Technical Data
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Background References
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Effect of 6-hydroxyDA on brain NE and DA: evidence for selective degeneration of catecholamine neurons.
Breese and Traylor
J.Pharmacol.Exp.Ther., 1970;174:413 -
Autoxidation and neurotoxicity of 6-hydroxyDA in the presence of some antioxidants: potential implication in relation to the pathogenesis of Parkinson's disease.
Soto-Otero et al.
J.Neurochem., 2000;74:1605 -
Cell-permeable cAMP analog suppresses 6-hydroxyDA-induced apoptosis in PC12 cells through the activation of the Akt pathway.
Fujita et al.
Brain Res., 2006;1113:10
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Citations for 6-Hydroxydopamine hydrobromide
The citations listed below are publications that use Tocris products. Selected citations for 6-Hydroxydopamine hydrobromide include:
10 Citations: Showing 1 - 10
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External light activates hair follicle stem cells through eyes via an ipRGC-SCN-sympathetic neural pathway.
Authors: Fan
Proc Natl Acad Sci U S A. 2018;115(29):E6880
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CRO reduces L-dopa-induced dyskinesia severity in 6-hydroxyDA parkinson's disease model.
Authors: Chotibut Et al.
Mov Disord 2017;32:1547
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Assessment of the Protection of DArgic Neurons by an α7 Nicotinic Receptor Agonist, PHA 543613 Using [(18)F]LBT-999 in a Parkinson's Disease Rat Model.
Authors: Sérriàre Et al.
PLoS One 2015;2:61
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Mitochondrial dysfunction, oxidative stress, and neurodegeneration elicited by a bacterial metabolite in a C. elegans Parkinson's model.
Authors: Ray Et al.
Cell Death Dis 2014;5:e984
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Derivation and expansion using only small molecules of human neural progenitors for neurodegenerative disease modeling.
Authors: Reinhardt Et al.
Neural Plast 2013;8:e59252
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ER stress inhibits neuronal death by promoting autophagy.
Authors: Fouillet Et al.
Front Med (Lausanne) 2012;8:915
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Use of PC12 cells and rat superior cervical ganglion sympathetic neurons as models for neuroprotective assays relevant to Parkinson's disease.
Authors: Grau and Greene
Methods Mol Biol 2012;846:201
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Suppression of bladder overactivity by adenosine A2A receptor antagonist in a rat model of Parkinson disease.
Authors: Kitta Et al.
J Urol 2012;187:1890
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Rapamycin protects against neuron death in in vitro and in vivo models of Parkinson's disease.
Authors: Malagelada Et al.
J Neurosci 2010;30:1166
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RTP801 is induced in Parkinson's disease and mediates neuron death by inhibiting Akt phosphorylation/activation.
Authors: Malagelada Et al.
J Neurosci 2008;28:14363
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I used the 6-Hydroxydopamine (6-OHDA) to deplete dopaminergic cells from the mouse brain, which is largely used as an experimental model of Parkinson's Disease. The 6-OHDA was injected into the mouse striatum and 21 days later we observed that the dopaminergic neurons (positive for tyrosine hydroxylase immunofluorescence) were almost absent in the substantia nigra pars compacta (SNc) from the 6-OHDA injected hemisphere (on the left). As a control for analytical comparisons, we also injected PBS into the contralateral hemisphere (on the right). When this neurotoxin is injected into striatum, as in this case, there is only a slight depletion of dopaminergic neurons from the ventral tegmental area (the region located into the middle of the image). The animals injected with 6-OHDA display several motor dysfunctions and are used to study the pathology and therapies for Parkinsonian symptoms.
