A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.

Astrocyte-specific expression of tyrosine hydroxylase after intracerebral gene transfer induces behavioral recovery in experimental parkinsonism. (1/890)

Parkinson's disease is a neurodegenerative disorder characterized by the depletion of dopamine in the caudate putamen. Dopamine replacement with levodopa, a precursor of the neurotransmitter, is presently the most common treatment for this disease. However, in an effort to obtain better therapeutic results, tissue or cells that synthesize catecholamines have been grafted into experimental animals and human patients. In this paper, we present a novel technique to express tyrosine hydroxylase (TH) in the host's own astrocytes. This procedure uses a transgene in which the expression of a TH cDNA is under the control of a glial fibrillary acidic protein (GFAP) promoter, which confers astrocyte-specific expression and also increases its activity in response to brain injury. The method was tested in a rat model of Parkinson's disease produced by lesioning the striatum with 6-hydroxydopamine. Following microinjection of the transgene into the denervated striatum as a DNA-liposome complex, expression of the transgene was detected by RT-PCR and TH protein was observed specifically in astrocytes by using double-labeling immunofluorescence for GFAP and TH coupled with laser confocal microscopy. Efficacy was demonstrated by significant behavioral recovery, as assessed by a decrease in the pharmacologically induced turning behavior generated by the unilateral denervation of the rat striatum. These results suggest this is a valuable technique to express molecules of therapeutic interest in the brain.  (+info)

Effect of central corticotropin-releasing factor on carbon tetrachloride-induced acute liver injury in rats. (2/890)

Central neuropeptides play important roles in many instances of physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Stressors and sympathetic nerve activation are reported to exacerbate experimental liver injury. Some stressors are known to stimulate corticotropin-releasing factor (CRF) synthesis in the central nervous system and induce activation of sympathetic nerves in animal models. The effect of intracisternal CRF on carbon tetrachloride (CCl4)-induced acute liver injury was examined in rats. Intracisternal injection of CRF dose dependently enhanced elevation of the serum alanine aminotransferase (ALT) level induced by CCl4. Elevations of serum aspartate aminotransferase, alkaline phosphatase, and total bilirubin levels by CCl4 were also enhanced by intracisternal CRF injection. Intracisternal injection of CRF also aggravated CCl4-induced hepatic histological changes. Intracisternal CRF injection alone did not modify the serum ALT level. Intravenous administration of CRF did not influence CCl4-induced acute liver injury. The aggravating effect of central CRF on CCl4-induced acute liver injury was abolished by denervation of hepatic plexus with phenol and by denervation of noradrenergic fibers with 6-hydroxydopamine treatment but not by hepatic branch vagotomy or atropine treatment. These results suggest that CRF acts in the brain to exacerbate acute liver injury through the sympathetic-noradrenergic pathways.  (+info)

Developmental regulation of expression of the D3 dopamine receptor in rat nucleus accumbens and islands of Calleja. (3/890)

The dopamine D3 receptor (D3R) belongs to the D2 subfamily and is expressed in the rat brain in targets of the mesolimbic dopaminergic system. Little is known about its normal development and control by dopaminergic innervation. We studied developmental expression of D3R in the rat nucleus accumbens (NAC) and islands of Calleja (ISC). At postnatal day (P) 7, D3 binding sites and mRNA were low in both areas. By P14, D3R and mRNA concentrations were close to adult levels in the ISC, whereas, in the NAC, binding increased until 3 months after birth. Cellular concentrations of D3 mRNA in the ISC increased with age in conjunction with a decrease in the number of D3 positive cells. In the NAC, the number of positive cells increased, whereas cellular levels of expression remained unchanged. Neonatal 6-hydroxydopamine lesion caused age-dependent changes in D3R expression. D3 binding sites did not change at P7 or P14, but there was a reduction in the number of D3 mRNA positive neurons accompanied by an increase in cellular levels of D3 mRNA at P14, suggesting that changes occurred in a subset of neurons. Up-regulation of D3 binding sites in NAC and ISC occurred 1 month after the lesion (P35) concomitant with a decrease in cellular levels of D3 mRNA and the number of D3 mRNA positive cells. At 3 months (P90) after the lesion, an increase in D3 mRNA occurred with no change in D3 binding sites. D3R shows region-specific dynamics in receptor/mRNA expression during development and is sensitive to loss of dopamine in early postnatal development.  (+info)

Herpes simplex virus vector-mediated expression of Bcl-2 prevents 6-hydroxydopamine-induced degeneration of neurons in the substantia nigra in vivo. (4/890)

6-Hydroxydopamine (6-OHDA) is widely used to selectively lesion dopaminergic neurons of the substantia nigra (SN) in the creation of animal models of Parkinson's disease. In vitro, the death of PC-12 cells caused by exposure to 6-OHDA occurs with characteristics consistent with an apoptotic mechanism of cell death. To test the hypothesis that apoptotic pathways are involved in the death of dopaminergic neurons of the SN caused by 6-OHDA, we created a replication-defective genomic herpes simplex virus-based vector containing the coding sequence for the antiapoptotic peptide Bcl-2 under the transcriptional control of the simian cytomegalovirus immediate early promoter. Transfection of primary cortical neurons in culture with the Bcl-2-producing vector protected those cells from naturally occurring cell death over 3 weeks. Injection of the Bcl-2-expressing vector into SN of rats 1 week before injection of 6-OHDA into the ipsilateral striatum increased the survival of neurons in the SN, detected either by retrograde labeling of those cells with fluorogold or by tyrosine hydroxylase immunocytochemistry, by 50%. These results, demonstrating that death of nigral neurons induced by 6-OHDA lesioning may be blocked by the expression of Bcl-2, are consistent with the notion that cell death in this model system is at least in part apoptotic in nature and suggest that a Bcl-2-expressing vector may have therapeutic potential in the treatment of Parkinson's disease.  (+info)

Enhancement of (-)-stepholidine on protein phosphorylation of a dopamine- and cAMP-regulated phosphoprotein in denervated striatum of oxidopamine-lesioned rats. (5/890)

AIM: To study effects of (-)-stepholidine (SPD) on the phosphorylation of a dopamine- and cAMP-regulated phosphoprotein (DARPP-32) in the striatum of oxidopamine-lesioned rats. METHODS: The amount of dephospho-DARPP-32 was measured by a back-phosphorylation assay. RESULTS: In the striatum of control rats, SPD per se had no effect on the phosphorylation of DARPP-32, but it antagonized the decrease by 28% of dephospho-DARPP-32 induced by the D1 agonist SK&F-38393. In the denervated striatum of oxidopamine-lesioned rats, SPD decreased the amount of dephospho-DARPP-32 by 44%. The effect of SPD was completely counteracted by the concomitant administration of the D1 antagonist Sch-23390. CONCLUSION: SPD exhibits D1 agonistic action on DARPP-32 phosphorylation in the denervated striatum of oxidopamine-lesioned rats, but it acts as a D1 antagonist in normal striatum.  (+info)

Rat strain differences in the ability to disrupt sensorimotor gating are limited to the dopaminergic system, specific to prepulse inhibition, and unrelated to changes in startle amplitude or nucleus accumbens dopamine receptor sensitivity. (6/890)

Previous studies indicate that a variety of pharmacological agents interfere with the prepulse inhibition of the acoustic startle (PPI) response including phencyclidine (PCP), 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), amphetamine, and apomorphine. Strain differences have been observed in the ability of apomorphine to disrupt PPI, although the degree to which these strain differences occur after administration of nondopaminergic drugs or the degree to which differences can be observed in other models of dopamine (DA) receptor activation has not been elucidated. The present study tested the effects of apomorphine, amphetamine, 8-OH-DPAT, and PCP on PPI in the Sprague Dawley and Wistar rat strains. Because apomorphine disrupts PPI via activation of DA receptors in the nucleus accumbens, apomorphine-induced hyperlocomotion, also a behavioral model of nucleus accumbens DA receptor activation, was measured in both rat strains. Administration of PCP or 8-OH-DPAT attenuated PPI in both strains, whereas apomorphine and amphetamine only attenuated PPI in Wistar rats. The ability of apomorphine to increase motor activity in the absence of a startle-eliciting stimulus was similar in the two strains, as was apomorphine-induced hyperlocomotion. A time course analysis of the effects of apomorphine on startle response in Sprague Dawley rats found that changes in the magnitude of PPI followed changes in basic startle amplitude. Similarly, no apomorphine-induced attenuation of PPI was observed in Sprague Dawley rats after 6-OHDA-induced DA receptor supersensitivity in the nucleus accumbens. These data suggest a dissociation between the effects of DA receptor agonists in PPI and other behavioral models of DA receptor activation.  (+info)

Total neurochemical lesion of noradrenergic neurons of the locus ceruleus does not alter either naloxone-precipitated or spontaneous opiate withdrawal nor does it influence ability of clonidine to reverse opiate withdrawal. (7/890)

It has been suggested that an increase firing rate of noradrenergic neurons of the locus ceruleus is responsible for the opiate withdrawal syndrome. However, lesion studies have indicated that the noradrenergic neurons of the locus ceruleus are not essential for either the expression or suppression by clonidine of opiate withdrawal. The present study was designed to determine the effect of the almost complete 6-hydroxydopamine lesion of noradrenergic neurons (94%) of the locus ceruleus on various components of the opiate withdrawal syndrome and on its protection by clonidine. Morphine dependence was induced by s.c. implantation of morphine pellets (2 x 75 mg base). The following paradigms were used: 1) naloxone-induced conditioned place aversion, 2) naloxone-precipitated acute opiate withdrawal syndrome, 3) nycthemeral locomotor activity as a measure of spontaneous opiate withdrawal. The results showed that quasi-total lesion of noradrenergic neurons of the locus ceruleus did not modify opiate dependence as revealed by naloxone-induced conditioned place aversion and the expression of an acute morphine withdrawal syndrome. Moreover, clonidine prevented the opiate withdrawal syndrome in both lesioned and sham-operated rats, suggesting that the action of clonidine is certainly mediated through postsynaptic alpha(2)-adrenoceptor stimulation. Finally, the nycthemeral locomotor activity during spontaneous morphine withdrawal did not differ between the lesioned and the sham-operated rats.  (+info)

Sympathectomy inhibits the vasoactive effects of nicotine in conscious rats. (8/890)

OBJECTIVE: The mechanisms underlying the pressor response to nicotine are incompletely understood. Although sympatho-adrenergic activation plays a major role, the relative contribution of adrenal vs. neurally released catecholamines and the possible role of non-adrenergic factors (e.g. vasopressin release) is not established. METHODS: We examined the cardiovascular responses to graded i.v. injections of nicotine (1 to 100 micrograms kg-1) in conscious Wistar-Kyoto rats under control conditions and (i) after chemical sympathectomy by 6-hydroxydopamine, which destroys sympathetic endings but spares the adrenal medulla; (ii) after an alpha-adrenergic blockade by phenoxybenzamine; (iii) after a V1 vasopressin receptor blockade by a specific antagonist. RESULTS: In control rats, nicotine caused a dose-dependent tachycardiac and pressor response. Both responses were abolished by sympathectomy, whereas the alpha-blockade left the tachycardiac response unaffected but inhibited the pressor response: the V1 vasopressin receptor blockade had no effect on either the tachycardiac or pressor response. CONCLUSIONS: We conclude that in the conscious rat; (1) the pressor response to nicotine mainly depends on peripheral alpha-adrenergically-mediated vasoconstriction; (2) the vasomotor effect is caused by neural rather than adrenomedullary catecholamine release; (3) the nicotine-induced increase in heart rate (and presumably cardiac output) is per se unable to raise blood pressure, and (4) the nicotine-induced release of vasopressin plays no significant role in the pressor response.  (+info)

Oxidopamine is not a recognized medical term or a medication commonly used in clinical practice. However, it is a chemical compound that is often used in scientific research, particularly in the field of neuroscience.

Oxidopamine is a synthetic catecholamine that can be selectively taken up by dopaminergic neurons and subsequently undergo oxidation, leading to the production of reactive oxygen species. This property makes it a useful tool for studying the effects of oxidative stress on dopaminergic neurons in models of Parkinson's disease and other neurological disorders.

In summary, while not a medical definition per se, oxidopamine is a chemical compound used in research to study the effects of oxidative stress on dopaminergic neurons.

... is a primary amino compound, a benzenetriol and a catecholamine. The molecular weight of this oxidopamine is 169.18 ... The neurontoxin oxidopamine has first been described in 1959. Years later, in 1968 the first model exploiting oxidopamine ... The toxin oxidopamine is a relatively unstable compound. In certain experimental conditions, oxidopamine will undergo ... "Oxidopamine". pubchem.ncbi.nlm.nih.gov. Retrieved 2022-03-04. "Oxidopamine - an overview , ScienceDirect Topics". www. ...
5,7-Dihydroxytryptamine MPTP Oxidopamine Daw NW, Videen TO, Parkinson D, Rader RK (1985). "DSP-4 (N-(2-Chloroethyl)-N-ethyl-2- ...
... may refer to: 2-Hydroxydopamine 5-Hydroxydopamine [Wikidata] 6-Hydroxydopamine (oxidopamine) This set index ...
Oxidopamine (6-hydroxydopamine) XP21279 A photoswitchable agonist of D1-like receptors (azodopa) has been described that allows ...
Bethanidine Bretylium Guanadrel Guanazodine Guanclofine Guanethidine Guanoxan Oxidopamine (6-hydroxydopamine) Prischich, Davia ...
oxetorone (INN) oxfendazole (INN) oxfenicine (INN) oxibendazole (INN) oxibetaine (INN) oxiconazole (INN) oxidopamine (INN) ...
... oxidopamine MeSH D02.092.311.461 - epinephrine MeSH D02.092.311.461.200 - deoxyepinephrine MeSH D02.092.311.461.400 - ...
... or noradrenaline Oxidopamine, a dopamine derivative Pyridoxine This set index page lists chemical structure articles associated ...
... and oxidopamine-induced neuronal injury. Omigapil also prevents the death of nigrostriatal dopaminergic neurons in monkeys ...
Oxidopamine is a primary amino compound, a benzenetriol and a catecholamine. The molecular weight of this oxidopamine is 169.18 ... The neurontoxin oxidopamine has first been described in 1959. Years later, in 1968 the first model exploiting oxidopamine ... The toxin oxidopamine is a relatively unstable compound. In certain experimental conditions, oxidopamine will undergo ... "Oxidopamine". pubchem.ncbi.nlm.nih.gov. Retrieved 2022-03-04. "Oxidopamine - an overview , ScienceDirect Topics". www. ...
This is an historical archive of the activities of the MRC Anatomical Neuropharmacology Unit (MRC ANU) that operated at the University of Oxford from 1985 until March 2015. The MRC ANU established a reputation for world-leading research on the brain, for training new generations of scientists, and for engaging the general public in neuroscience. The successes of the MRC ANU are now built upon at the MRC Brain Network Dynamics Unit at the University of Oxford.. ...
Oxidopamine * Parkinsonian Disorders / drug therapy * Parkinsonian Disorders / pathology * Parkinsonian Disorders / ...
Dive into the research topics of Riluzole neuroprotection in a parkinsons disease model involves suppression of reactive astrocytosis but not GLT-1 regulation. Together they form a unique fingerprint. ...
Tsai, C-Y., Lin, Y., Liu, W-T., Cheong, H., Houghton, R., Hsu, W-H., Iulia, M., Liu, Y-S., Kang, J-H., Lee, K-Y., Kuan, Y-C., Lee, H-C., Wu, C-J., Li, L-Y. J., Cheng, W-H., Ho, S-C., Lin, S-Y. & Majumdar, A., 2023, In: Transportation Research Record. 0, 0, p. 03611981221123802 1 p.. Research output: Contribution to journal › Article › peer-review ...
Hartung, T., Smirnova, L., Morales Pantoja, I. E., Akwaboah, A., Alam El Din, D-M., Berlinicke, C. A., Boyd, J. L., Caffo, B. S., Cappiello, B., Cohen-Karni, T., Curley, J. L., Etienne-Cummings, R., Dastgheyb, R., Gracias, D. H., Gilbert, F., Habela, C. W., Han, F., Harris, T. D., Herrmann, K., Hill, E. J., & 23 othersHuang, Q., Jabbour, R. E., Johnson, E. C., Kagan, B. J., Krall, C., Levchenko, A., Locke, P., Maertens, A., Metea, M., Muotri, A. R., Parri, R., Paulhamus, B. L., Plotkin, J. D., Roach, P., Romero, J. C., Schwamborn, J. C., Sillé, F., Szalay, A. S., Tsaioun, K., Tornero, D., Vogelstein, J. T., Wahlin, K. J. & Zack, D. J., 28 Feb 2023, (E-pub ahead of print) In: Frontiers in Science. 3 p.. Research output: Contribution to journal › Editorial › peer-review ...
Oxidopamine Medicine & Life Sciences 75% * Dopaminergic Neurons Medicine & Life Sciences 68% * Beta-Lactam Antibiotic Chemical ...
Oxidopamine. A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of ... Molecular Motor ProteinsProton-Translocating ATPasesBacterial Proton-Translocating ATPasesAdenosine TriphosphateOxidopamine ...
Oxidopamine. A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of ... muLearningBasal GangliaDopamine AgonistsOxidopamineHaloperidolSynapsesRats, Sprague-DawleySynaptic TransmissionMicroscopy, ... muDopamine AgonistsOxidopamineHaloperidolGlutamic Acidgamma-Aminobutyric AcidReceptors, N-Methyl-D-Aspartate ...
Yamashita, T., Ono, K., Ohuchi, H., Yumoto, A., Gotoh, H., Tomonari, S., Sakai, K., Fujita, H., Imamoto, Y., Noji, S., Nakamura, K. & Shichida, Y., Feb 14 2014, In: Journal of Biological Chemistry. 289, 7, p. 3991-4000 10 p.. Research output: Contribution to journal › Article › peer-review ...
Dive into the research topics of Polysomnographic features of sleep disturbances and rem sleep behavior disorder in the unilateral 6-OHDA lesioned hemiparkinsonian rat. Together they form a unique fingerprint. ...
Chen, C. Z., Sheu, C. C., Cheng, S. L., Wang, H. C., Lin, M. C., Hsu, W. H., Lee, K. Y., Perng, D. W., Lin, H. I., Lin, M. S., Lin, S. H., Tsai, J. R., Wang, C. C., Wang, C. Y., Yang, T. M., Liu, C. L., Wang, T. Y. & Lin, C. H., Jan 1 2021, In: International journal of chronic obstructive pulmonary disease. 16, p. 3405-3415 11 p.. Research output: Contribution to journal › Article › peer-review ...
Goedert, M., Lightman, S. L., Mantyh, P. W., Hunt, S. P. & Emson, P. C., Dec 9 1985, In: Brain Research. 358, 1-2, p. 59-69 11 p.. Research output: Contribution to journal › Article › peer-review ...
Barker, R. A., Farrell, K., Guzman, N. V., He, X., Lazic, S. E., Moore, S., Morris, R., Tyers, P., Wijeyekoon, R., Daft, D., Hewitt, S., Dayal, V., Foltynie, T., Kefalopoulou, Z., Mahlknecht, P., Lao-Kaim, N. P., Piccini, P., Bjartmarz, H., Björklund, A., Lindvall, O., & 13 othersNelander-Wahlestedt, J., Parmar, M., Paul, G., Widner, H., Church, A., Dunnett, S., Peall, K., Rosser, A., Gurruchaga, J. M., Palfi, S., Piroth, T., Winkler, C. & TRANSEURO consortium, 2019 Jul, In: Nature Medicine. 25, p. 1045-1053 9 p.. Research output: Contribution to journal › Article › peer-review ...
Cui Zhou, D., Jayasinghe, R. G., Chen, S., Herndon, J. M., Iglesia, M. D., Navale, P., Wendl, M. C., Caravan, W., Sato, K., Storrs, E., Mo, C. K., Liu, J., Southard-Smith, A. N., Wu, Y., Naser Al Deen, N., Baer, J. M., Fulton, R. S., Wyczalkowski, M. A., Liu, R., Fronick, C. C., & 46 othersFulton, L. A., Shinkle, A., Thammavong, L., Zhu, H., Sun, H., Wang, L. B., Li, Y., Zuo, C., McMichael, J. F., Davies, S. R., Appelbaum, E. L., Robbins, K. J., Chasnoff, S. E., Yang, X., Reeb, A. N., Oh, C., Serasanambati, M., Lal, P., Varghese, R., Mashl, J. R., Ponce, J., Terekhanova, N. V., Yao, L., Wang, F., Chen, L., Schnaubelt, M., Lu, R. J. H., Schwarz, J. K., Puram, S. V., Kim, A. H., Song, S. K., Shoghi, K. I., Lau, K. S., Ju, T., Chen, K., Chatterjee, D., Hawkins, W. G., Zhang, H., Achilefu, S., Chheda, M. G., Oh, S. T., Gillanders, W. E., Chen, F., DeNardo, D. G., Fields, R. C. & Ding, L., Sep 2022, In: Nature Genetics. 54, 9, p. 1390-1405 16 p.. Research output: Contribution to journal › Article ...
Hsieh, T. H., He, X. K., Liu, H. H., Chen, J. J. J., Peng, C. W., Liu, H. L., Rotenberg, A., Chen, K. T., Chang, M. Y., Chiang, Y. H., Chang, P. K. & Kuo, C. W., 2021, In: Neural Plasticity. 2021, 1763533.. Research output: Contribution to journal › Article › peer-review ...
Dive into the research topics of Cardiovascular regulation after destruction of the C1 cell group of the rostral ventrolateral medulla in rats. Together they form a unique fingerprint. ...
Ken Kuwahara, Tatsuya Sasaki, Takao Yasuhara, Masahiro Kameda, Yosuke Okazaki, Kakeru Hosomoto, Ittetsu Kin, Mihoko Okazaki, Satoru Yabuno, Satoshi Kawauchi, Yousuke Tomita, Michiari Umakoshi, Kyohei Kin, Jun Morimoto, Jea Young Lee, Naoki Tajiri, Cesar V. Borlongan, Isao Date ...
DILLION, G., Koulen, P., SIMPKINS, J., SUMIEN, N., SIMPKINS, J., DILLION, G., Koulen, P., SUMIEN, N., Singh, M., Forster, M. & FORSTER, M.. National Institute on Aging. 30/09/03 → 29/02/16. Project: Research ...
Oxidopamine (6-Hydroxydopamine) ...
Oxidopamine Medicine & Life Sciences 28% * Kidney Medicine & Life Sciences 26% * Clonazepam Chemical Compounds 18% ...
Oxidopamine Medicine & Life Sciences 30% * In Vitro Techniques Medicine & Life Sciences 23% ...
Oxidopamine Medicine & Life Sciences 100% * Dopaminergic Neurons Medicine & Life Sciences 90% * Nuclear Receptor Subfamily 4, ...
Oxidopamine Medicine & Life Sciences 25% * Enzyme Inhibitors Medicine & Life Sciences 24% * Catecholamines Medicine & Life ...
Oxidopamine Medicine & Life Sciences 86% * Microtubules Medicine & Life Sciences 73% * Parkinson Disease Medicine & Life ...
Oxidopamine*Oxidopamine hydrochloride*Oxifenbutazona [INN-Spanish]*Oxifenon*Oxifenylbutazon*Oxigenal*Oxigeno [Spanish]* ...
https://www.selleckchem.com/products/oxidopamine-hydrobromide.html. Sex:. *Female. sailbarge6s Signature. ...
GO:1905848 positive regulation of cellular response to oxidopamine * GO:1903846 positive regulation of cellular response to ... positive regulation of cellular response to oxidopamine (GO:1905848) is_a positive regulation of response to stimulus ...
In this concept cloud, the sizes of the concepts are based not only on the number of corresponding publications, but also how relevant the concepts are to the overall topics of the publications, how long ago the publications were written, whether the person was the first or senior author, and how many other people have written about the same topic. The largest concepts are those that are most unique to this person ...
Levodopa inhibits the reaction [Oxidopamine results in decreased expression of PDYN mRNA]. R ... Levodopa promotes the reaction [Oxidopamine results in increased expression of PENK mRNA]. R ...
  • Oxidopamine, also known as 6-hydroxydopamine (6-OHDA) or 2,4,5-trihydroxyphenethylamine, is a neurotoxic synthetic organic compound used by researchers to selectively destroy dopaminergic and noradrenergic neurons in the brain. (wikipedia.org)
  • The main use for oxidopamine in scientific research is to induce Parkinsonism in laboratory animals by lesioning the dopaminergic neurons of the substantia nigra pars compacta, in order to develop and test new medicines and treatments for Parkinson's disease. (wikipedia.org)
  • Oxidopamine is taken up by and accumulates in catecholaminergic neurons. (wikipedia.org)
  • In order to induce Parkinsonism in animals, around 70% of the dopaminergic neurons in the substantia nigra of the brain must be destroyed, and this is often achieved either with oxidopamine or another neurotoxin MPTP. (wikipedia.org)
  • Oxidopamine is often used in conjunction with a selective noradrenaline reuptake inhibitor (such as desipramine) to selectively destroy dopaminergic neurons. (wikipedia.org)
  • Therefore oxidopamine can induce Parkinson disease in animal models. (wikipedia.org)
  • Ever since, oxidopamine has become an abundantly used neurotoxin for making animal models with Parkinson's disease. (wikipedia.org)
  • The toxin oxidopamine, an antagonist of the neurotransmitter dopamine, and is commonly used for making experimental animal models in Parkinson's disease. (wikipedia.org)
  • Within the neuron, oxidopamine is oxidized by monoamine oxidase producing the toxic products hydrogen peroxide (H2O2), catecholamine quinones and reactive oxygen species (ROS). (wikipedia.org)