Oxidopamine hydrochloride - CAS 28094-15-7
Catalog number: 28094-15-7
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Dopamine Receptor
Oxidopamine hydrochloride, also called as 6-OHDA, is a selective catecholaminergic neurotoxin that selectively destroy dopaminergic and noradrenergic neurons in the brain.
Beige solid
5-(2-aminoethyl)benzene-1,2,4-triol;hydrochloride 6 Hydroxydopamine 6-Hydroxydopamine 6-OHDA Hydrobromide, Oxidopamine Hydrochloride, Oxidopamine Oxidopamine Oxidopamine Hydrobromide Oxidopamine Hydrochloride
Soluble to 32mg/mL in DMSO
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -23℃ for long term (months to years).
Shelf Life:
2 years
Canonical SMILES:
1.Effect of depletion of spinal noradrenaline by 6-hydroxydopamine on the development of renal hypertension in rats.
Bosland MC;Versteeg DH;van Put J;de Jong W Clin Exp Pharmacol Physiol. 1981 Jan;8(1):67-77.
1. A single injection in rats of 250 microgram of 6-hydroxydopamine HCl (6-OHDA) into the subarachnoidal space of the spinal cord of rats resulted in a lasting, selective depletion of spinal noradrenaline. Dopamine levels in the spinal cord and catecholamine levels in various brain regions were not markedly affected. 2. When ether anesthesia was used spinal noradrenaline was found to be almost completely depleted by the administration of 6-OHDA. Only partial depletion was achieved when pentobarbitone anaesthesia or neuroleptic analgesia was used. 3. The blood pressure rise caused by electrical stimulation of the posterior hypothalamus was not affected by 6-OHDA treatment 7 days previously. 4. 6-OHDA administration did not influence the development of two-kidney Goldblatt hypertension. When 6-OHDA was administered 7 days before clipping, a slight delay of the development was observed, but this did not occur when 6-OHDA treatment was given 3--4 h before clipping. 5. It is concluded that intact spinal noradrenergic neurotransmission is neither a prerequisite for the development of two-kidney Goldblatt hypertension, nor for the pressor response to hypothalamic stimulation.
2.Small molecule inhibition of RISC loading.
Tan GS;Chiu CH;Garchow BG;Metzler D;Diamond SL;Kiriakidou M ACS Chem Biol. 2012 Feb 17;7(2):403-10. doi: 10.1021/cb200253h. Epub 2011 Nov 11.
Argonaute proteins are the core components of the microRNP/RISC. The biogenesis and function of microRNAs and endo- and exo- siRNAs are regulated by Ago2, an Argonaute protein with RNA binding and nuclease activities. Currently, there are no in vitro assays suitable for large-scale screening of microRNP/RISC loading modulators. We describe a novel in vitro assay that is based on fluorescence polarization of TAMRA-labeled RNAs loaded to human Ago2. Using this assay, we identified potent small-molecule inhibitors of RISC loading, including aurintricarboxylic acid (IC(50) = 0.47 μM), suramin (IC(50) = 0.69 μM), and oxidopamine HCL (IC(50) = 1.61 μM). Small molecules identified by this biochemical screening assay also inhibited siRNA loading to endogenous Ago2 in cultured cells.
3.Synaptic morphology in the neostriatum of the rat: Possible serotonergic synapse.
Hattori T;McGeer PL;McGeer EG Neurochem Res. 1976 Oct;1(5):451-67. doi: 10.1007/BF00964209.
Electron-microscopic examination of the striatum of rats 2-3 days after intraperitoneal injection of 10-15 mg/kgp-chloroamphetamine (PCA) indicated two types of terminal degeneration: a light, filamentous degeneration of symmetrical boutons, and a dark, electron-dense degeneration of asymmetrical boutons. The latter was identical to that seen 2-3 days after 6-hydroxydopamine hydrochloride (6-OHDA), and its frequency after PCA was decreased if the animal had been pretreated 10 days previously with 6-OHDA. The same two morphological types of striatal synapses were preferentially labeled by intraventricularly administered [(3)H]5-HT. No structural specificity in labeling in the striatum was seen after raphe injections of labeled 5-HTP or 5-HT. The probable morphology of striatal dopaminergic, cholinergic, GABAnergic, and serotonergic synapses is discussed, with a review of the pertinent evidence.
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