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.
|Storage||Desiccate at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 250.09. Batch specific molecular weights may vary from batch to batch due to solvent of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||4 mL||19.99 mL||39.99 mL|
|5 mM||0.8 mL||4 mL||8 mL|
|10 mM||0.4 mL||2 mL||4 mL|
|50 mM||0.08 mL||0.4 mL||0.8 mL|
The reconstitution calculator allows you to quickly calculate the volume of a reagent to reconstitute your vial. Simply enter the mass of reagent and the target concentration and the calculator will determine the rest.
References are publications that support the products' biological activity.
Breese and Traylor (1970) Effect of 6-hydroxydopamine on brain norepinephrine and dopamine: evidence for selective degeneration of catecholamine neurons. J.Pharmacol.Exp.Ther. 174 413 PMID: 5456173
Soto-Otero et al (2000) Autoxidation and neurotoxicity of 6-hydroxydopamine in the presence of some antioxidants: potential implication in relation to the pathogenesis of Parkinson's disease. J.Neurochem. 74 1605 PMID: 10737618
Fujita et al (2006) Cell-permeable cAMP analog suppresses 6-hydroxydopamine-induced apoptosis in PC12 cells through the activation of the Akt pathway. Brain Res. 1113 10 PMID: 16945353
If you know of a relevant reference for 6-Hydroxydopamine hydrobromide, please let us know.
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Keywords: Selective catecholaminergic neurotoxin Dopamine Receptors adrenoceptors adrenergic dopaminergic neurotoxins parkinson's parkinsons 6-OHDA Dopaminergic-Related
6 Citations for 6-Hydroxydopamine hydrobromide
Citations are publications that use Tocris products. Selected citations for 6-Hydroxydopamine hydrobromide include:
Sérriàre et al (2015) Assessment of the Protection of Dopaminergic Neurons by an α7 Nicotinic Receptor Agonist, PHA 543613 Using [(18)F]LBT-999 in a Parkinson's Disease Rat Model. PLoS One 2 61 PMID: 26389120
Reinhardt et al (2013) Derivation and expansion using only small molecules of human neural progenitors for neurodegenerative disease modeling. Neural Plast 8 e59252 PMID: 23533608
Grau and Greene (2012) Use of PC12 cells and rat superior cervical ganglion sympathetic neurons as models for neuroprotective assays relevant to Parkinson's disease. Methods Mol Biol 846 201 PMID: 22367813
Fouillet et al (2012) ER stress inhibits neuronal death by promoting autophagy. Front Med (Lausanne) 8 915 PMID: 22660271
Malagelada et al (2010) Rapamycin protects against neuron death in in vitro and in vivo models of Parkinson's disease. J Neurosci 30 1166 PMID: 20089925
Malagelada et al (2008) RTP801 is induced in Parkinson's disease and mediates neuron death by inhibiting Akt phosphorylation/activation. J Neurosci 28 14363 PMID: 19118169
Do you know of a great paper that uses 6-Hydroxydopamine hydrobromide from Tocris? If so please let us know.
Literature in this Area
Dopamine Receptors Scientific Review
Written by Phillip Strange and revised by Kim Neve in 2013, this review summarizes the history of the dopamine receptors and provides an overview of individual receptor subtype properties, their distribution and identifies ligands which act at each receptor subtype. Compounds available from Tocris are listed.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.