988 resultados para L-Dopamine


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A flow injection method has been developed for the determination of dopamine based on its inhibition of the electrochemiluminescence of luminol. This method is simple and sensitive for dopamine detection. Under the selected experimental conditions, the decreased electrochemiluminescent intensity is linear with dopamine concentration in the range of 5.0 x 10(-8)-1.0 x 10(-5) mol/L with a detection limit of 30 nmol/L. The relative standard deviation of eleven determinations is 1.9% for 1.0 x 10(-6) mol/L dopamine. The proposed method has been applied to the detection of dopamine in pharmaceutical injections with satisfactory results.

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We have made a cheap microsystem of capillary electrophoresis with a new method, integrating the electrodes, injection channel, separation channel, buffer reservoirs and detection cell on a polymethylmethacrylate (PMMA) chip. Using an integrated micro carbon fiber disk electrode as the working electrode in three electrodes system, 1 x 10(-4) mol/L dopamine(DA) could be detected with end-column amperometric detection. The reproducibility was good. Peak current was 6.73 nA,theoretical plate number was 71300/m and height equivalent of one theoretical plate height was 14.0 mum for 1 x 10(-4) mol/L DA. The limit of detection was 3.6 x 10(-8) mol/L and the linear range was extended from 5 x 10(-7) mol/L to 1 x 10(-4) mol/L for DA. 1 x 10(-4) mol/L catechol (CA) and 5 x 10(-5) mol/L DA were also separated completely with R-s = 10.1.

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Imbalance between the dopamine and serotonin (5-HT) neurotransmitter systems has been implicated in the comorbidity of Parkinson's disease (PD) and psychiatric disorders. L-DOPA, the leading treatment of PD, facilitates the production and release of dopamine. This study assessed the action of L-DOPA on monoamine synaptic transmission in mouse brain slices. Application of L-DOPA augmented the D2-receptor-mediated inhibitory postsynaptic current (IPSC) in dopamine neurons of the substantia nigra. This augmentation was largely due to dopamine release from 5-HT terminals. Selective optogenetic stimulation of 5-HT terminals evoked dopamine release, producing D2-receptor-mediated IPSCs following treatment with L-DOPA. In the dorsal raphe, L-DOPA produced a long-lasting depression of the 5-HT1A-receptor-mediated IPSC in 5-HT neurons. When D2 receptors were expressed in the dorsal raphe, application of L-DOPA resulted in a D2-receptor-mediated IPSC. Thus, treatment with L-DOPA caused ectopic dopamine release from 5-HT terminals and a loss of 5-HT-mediated synaptic transmission.

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Effect of L-prolyl-cinagta tlheep spyo atenndt idaol paanmti-iPnaer/nkeinusroonleiapnti cp rreocpeeprttoiers b oifn dLi-npgrso.lyPl E-LP-TleIuDcEylS- g2l(y1c)Li n1-a0lem5u-ic1dy1el1-g,(Ply1Lc9iG8n1)a. mw-Taidhsee i nm(vPeeLcstGhiag) anotinesmd n ie onuf rb oaelchetapiovtinico -suuirnbadslu eacrnevddetnarflefetueeacrrtmto a coephfnp ePtrmLe(2icGc0iaa, lob4 mnl0y io atndnhedevl sii8tn r0oto fem dndgosoi ppktyaag mm o-1fii nn tSeehCr/eng cteiwcau tfiracuolenle edpcptattiiioiclcny r r feienoscrp et ohfpinetvos erer ad ebtali.iyncAsdit)cienusdgit ge bin nyai dfrhimacaatli nonsttpilrseytirar aiatdtuttoimeolnn u(a3aso tmfde PidgfL f hkeGargel -o(n'p2tI0ieaPr ali)ldn.y odB ll ay4-b 0icne omldlneugtdc rk eabgdsy t - c1,aa pcSthoaCrmleo)ponfrsaicypil .heP TidLn hteGoe pahnidn esp tior odpoepraimdoinl ew raesc aelpstoo ersx ainm tihnee dst.rPiaLtuGm s,elbeuctt ihvaedly n eon ehfafneccte don t h['eH a]ffsipniirtoyp oefr tidhoel sbpiencdifinicg .b Tinhdei nbge hoafv aigouonraislt an[3dH b] iaopcohmemori-- cal results obtained in the present study raise the possibility that PLG may facilitate nigro-striatal dopaminergic neurotransmission through interacting with a unique PLG receptor functionally coupled to the dopamine receptor cyclase complex. -adenylate

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The anionic complexes [Cu(L(1-))(3)](1-), L(-) = dopasemiquinone or L-dopasemiqui none, were prepared and characterized. The complexes are stable in aqueous solution showing intense absorption bands at ca. 605 nm for Cu(II)-L-dopasemiquinone and at ca. 595 nm for Cu(II)-dopasemiquinone in the UV-vis spectra, that can be assigned to intraligand transitions. Noradrenaline and adrenaline, under the same reaction conditions, did not yield Cu-complexes, despite the bands in the UV region showing that noradrenaline and adrenaline were oxidized during the process. The complexes display a resonance Raman effect, and the most enhanced bands involve ring modes and particularly the vCC + vCO stretching mode at ca. 1384 cm(-1). The free radical nature of the ligands and the oxidation state of the Cu(II) were confirmed by the EPR spectra that display absorptions assigned to organic radicals with g= 2.0005 and g = 2.0923, and for Cu(II) with g = 2.008 and g = 2.0897 for L-dopasemiquinone and dopasemiquinone, respectively. The possibility that dopamine and L-dopa can form stable and aqueous-soluble copper complexes at neutral pH, whereas noradrenaline and adrenaline cannot, may be important in understanding how Cu(II)-dopamine crosses the cellular membrane as proposed in the literature to explain the role of copper in Wilson disease. (c) 2008 Elsevier B.V. All rights reserved.

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BACKGROUND There is ample evidence that a subgroup of Parkinson's disease patients who are treated with dopaminergic drugs develop certain behavioral addictions such as pathological gambling. The fact that only a subgroup of these patients develops pathological gambling suggests an interaction between dopaminergic drug treatment and individual susceptibility factors. These are potentially of genetic origin, since research in healthy subjects suggests that vulnerability for pathological gambling may be linked to variation in the dopamine receptor D4 (DRD4) gene. Using a pharmacogenetic approach, we investigated how variation in this gene modulates the impact of dopaminergic stimulation on gambling behavior in healthy subjects. METHODS We administered 300 mg of L-dihydroxyphenylalanine (L-DOPA) or placebo to 200 healthy male subjects who were all genotyped for their DRD4 polymorphism. Subjects played a gambling task 60 minutes after L-DOPA administration. RESULTS Without considering genetic information, L-DOPA administration did not lead to an increase in gambling propensity compared with placebo. As expected, however, an individual's DRD4 polymorphism accounted for variation in gambling behavior after the administration of L-DOPA. Subjects who carry at least one copy of the 7-repeat allele showed an increased gambling propensity after dopaminergic stimulation. CONCLUSIONS These findings demonstrate that genetic variation in the DRD4 gene determines an individual's gambling behavior in response to a dopaminergic drug challenge. They may have implications for the treatment of Parkinson's disease patients by offering a genotype approach for determining individual susceptibilities for pathological gambling and may also afford insights into the vulnerability mechanisms underlying addictive behavior.

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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.

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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.

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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.

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Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.

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Utilizing a mono-specific antiserum produced in rabbits to hog kidney aromatic L-amino acid decarboxylase (AADC), the enzyme was localized in rat kidney by immunoperoxidase staining. AADC was located predominantly in the proximal convoluted tubules; there was also weak staining in the distal convoluted tubules and collecting ducts. An increase in dietary potassium or sodium intake produced no change in density or distribution of AADC staining in kidney. An assay of AADC enzyme activity showed no difference in cortex or medulla with chronic potassium loading. A change in distribution or activity of renal AADC does not explain the postulated dopaminergic modulation of renal function that occurs with potassium or sodium loading.

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Migraine is a common, genetically influenced neurovascular disorder. The dopamine transporter gene is a candidate for migraine association studies. This study tested a functionally linked variable number tandem repeat (VNTR) in intron 8 of the dopamine transporter gene (DATInt8) in 550 migraine cases (401 with aura, 149 without aura) and 550 non-migraine controls. Chi-squared analysis of the DATInt8 revealed that the allele and genotype frequency distributions for migraine cases (including subtype analysis) and controls were not different (P > 0.1). These findings offer no evidence for an association of the DATInt8 with migraine with and without aura and therefore do not implicate the dopamine transporter gene as a modifier of migraine risk.