Dopamine kinetics

The reuptake process does not capture all of the released catecholamine. Diffusion away from the nerve terminal to distant sites can occur and has been termed volume transmission [23]. Volume transmission allows the stimulation of extrasynaptic receptors, which has been described for dopamine [24] and norepinephrine [25]. Brain regions differ in their capacity for catecholamine reuptake thus, whereas extracellular dopamine concentrations are dominated by release in the cerebral cortex, in the striatum dopamine concentrations are dominated by reuptake [26]. These regional differences in extracellular dopamine kinetics correlate with levels of dopamine transporter [27]. 

Meiergerd SM, Patterson TA, Schenk JO (1993) D2 receptors may modulate the function of the striatal transporter for dopamine kinetic evidence from studies in vitro and in vivo. J Neurochem 61 764-7... 

Escribano, J. et al., Characterization of monophenolase activity of table beet polyphenol oxidase determination of kinetic parameters on the tyramine/dopamine pair, J. Agric. Food Ghem., 45, 4209, 1997. 

Amejdki-Chab, N., Costentin, J., and Bonnet, J. J., Kinetic analysis of the chloride dependence of the neuronal uptake of dopamine and effect of anions on the ability of substrates to compete with the binding of the dopamine uptake inhibitor GBR 12783, J. Neurochem., 58, 793, 1992. 

Krueger, B.K., Kinetics and block of dopamine uptake in synaptosomes from rat caudate nucleus, J. Neurochem., 55, 260, 1990. 

Sojo MM, Nunez-Delicado E, Sanchez-Ferrer A and Garcia-Carmona F. 2000. Oxidation of salsolinol by banana pulp polyphenol oxidase and its kinetic synergism with dopamine. J Agric Food Chem 48(11) 5543-5547. 

The effect of non-participating ligands on the copper catalyzed autoxidation of cysteine was studied in the presence of glycylglycine-phosphate and catecholamines, (2-R-)H2C, (epinephrine, R = CH(OH)-CH2-NHCH3 norepinephrine, R = CH(OH)-CH2-NH2 dopamine, R = CH2-CH2-NH2 dopa, R = CH2-CH(COOH)-NH2) by Hanaki and co-workers (68,69). Typically, these reactions followed Michaelis-Menten kinetics and the autoxidation rate displayed a bell-shaped curve as a function of pH. The catecholamines had no kinetic effects under anaerobic conditions, but catalyzed the autoxidation of cysteine in the following order of efficiency epinephrine = norepinephrine > dopamine > dopa. The concentration and pH dependencies of the reaction rate were interpreted by assuming that the redox active species is the [L Cun(RS-)] ternary complex which is formed in a very fast reaction between CunL and cysteine. Thus, the autoxidation occurs at maximum rate when the conditions are optimal for the formation of this species. At relatively low pH, the ternary complex does not form in sufficient concentration. 

Miller, S.M. and Klinman, J.P. (1982). Deduction of kinetic mechanisms from primary hydrogen isotope effects dopamine beta-monooxygenase - a case history. Methods Enzymol. 87, 711-732... 

Tian, G., Berry, J.A. and Khnman, J.P. (1994). Oxygen-18 kinetic isotope effects in the dopamine heta-monooxygenase reaction evidence for a new chemical mechanism in non-heme metaUomonooxygenases. Biochemistry 33, 226-234... 

Lepore, Marino, and Keith B. J. Franklin. 1992. "Modelling Drug Kinetics with Brain Stimulation Dopamine Antagonists Increase Self-Stimutation." Pharmacology Biochemistry and Behavior 41 489-96. 

The kinetic mechanism of the methylation reaction of human COMT has been studied exhaustively using recombinant enzymes [19]. The mechanism is sequential ordered AdoMet binding first, then Mg2+ and the catechol substrate as the last ligand. Human S-COMT and MB-COMT have similar kinetic properties. The main difference is the one-order lower Km value of MB-COMT for dopamine as substrate (S-COMT 207 pMand MB-COMT 15 pAT). The COMT enzyme is a rather slow enzyme with a low catalytic number. At saturating substrate levels S-COMT has a double efficiency compared with MB-COMT (kcat=37 and kcat =17, respectively). At low substrate concentrations (<10 iM) the MB-COMT seems to methylate catecholamines more rapidly than S-COMT. 

The type-3 copper of hemocyanins and tyrosinases is usually EPR silent with the exception e.g. of Helixpomatia methemocyanin. Dopamine P-monooxygenase has been described to contain only type-2 copper according to EPR data but there seems kinetic evidence for a transient binuclear site... 

The effects of ECP on dopamine (DA) and ascorbate (AA) voltammetry at physiological pH are illustrated in Figure 10.15. For both DA and AA on untreated fiber (curves A1 and Bl), slow kinetics cause a drawn-out oxidation... 

Flavin-containing mitochondrial MAO-A and MAO-B catalyze the oxidative deamination of neurotransmitters, such as dopamine, serotonin, and norepinephrine in the central nervous system and peripheral tissues. The enzymes share 73% sequence homology and follow the same kinetic and chemical mechanism but have different substrate and inhibitor specificities. Chemical modification experiments provide evidence that a histidine residue is essential for the catalysis. There is also strong evidence that two cysteine residues are present in the active site of MAO. 

Batchelor M, Schenk JO (1998) Protein kinase A activity may kinetically upregulate the striatal transporter for dopamine. J Neurosci 18 10304-9 Baumann PA, Waldmeier PC (1981) Further evidence for negative feedback control of serotonin release in the central nervous system. Naunyn-Schmiedeberg s Arch Pharmacol 317 36 13 Bean AJ, During MJ, Roth RH (1990) Effects of dopamine autoreceptor stimulation on the release of colocalized transmitters in vivo release of dopamine and neurotensin from rat prefrontal cortex. Neurosci Lett 108 143-8... 

Schmitz Y, Schmauss C, Sulzer D (2002) Altered dopamine release and uptake kinetics in mice lacking D2 receptors. J Neurosci 22 8002-9... 

SV detection was also achieved to detect catecholamines on a PDMS-quartz chip. Pyrolyzed photoresist films (PPF) were used as planar carbon electrodes. Since the photoresist (AZ4330) must adhere on a substrate for pyrolysis at 1000°C, a quartz plate that could withstand high temperature was selected. The LOD of dopamine decreased from 160 nM to 100 nM when the PPF was treated by piranha solution (HjSOyHjOj). It was because such a treatment increased the surface oxygen/carbon ratio, and hence the oxidation kinetics of dopamine wave improved [765]. 

In a related study [62], similar effects on conductivity of SWCNTs were reported, but here a comparison was also made between the effects of nitric acid reflux and air plasma treatment, and an attempt was made to relate the changes observed to the creation of defect sites. The authors did not offer a more concrete proposal regarding the nature of the sites involved in these treatments. After the acid treatment, Raman microscopy results indicated a dramatic change in SWNT electronic structure, and both treatments enhanced the electron transfer kinetics for the oxidation of inner-sphere dopamine. By contrast, both treatments had a negligible effect on the voltammetric response of a simple outer-sphere electron-transfer redox process Ru(NH3)63+/2+. ... 

In the in-vitro kinetic experiments, the rates of association (Kon) and dissociation (Kan) of various (labeled) antipsychotic compounds to dopamine D2 receptors were determined. Kapur and Seeman found that antipsychotics substantially differ (almost 1000-fold) in their Koff rate (whereas only 10-fold differences were found in the Kon rate), and that this value is highly correlated with their affinity to D2 receptors. These authors also demonstrated that Koff for clozapine, olanzapine and quetiapine was 1.386 min"1, 0.039 min"1, and 3.013 min"1, respectively, and assumed that the rate of how rapidly they left the receptor was an important mechanism in their atypical antipsychotic action. Indeed, this fully explained the lack of extrapyramidal symptoms (EPS) and hyperprolactinemia and the low risk for tardive dyskinesia [34—36]. In this regard, quetiapine (which has the lowest affinity to D2 receptors) seems to be the most atypical among all tested antipsychotics, followed by clozapine and olanzapine (nevertheless, olanzapine s Koff value is close to those of raclopride and chlorpromazine). 

Product inhibition kinetics performed at saturating levels of one substrate with norlaudanosoline as the inhibitor showed that NCS follows an iso-ordered biuni mechanism with 4-HPAA binding before dopamine (Fig.7.8). These data also imply that 4-HPAA combines with a form of the enzyme different from the alkaloid product since the inhibitor and first substrate do not bind competitively. After the product is released, NCS appears to undergo a conformational change reverting back to a form to which 4-HPAA can bind before another reaction sequence can begin.131... 

The stereospecific condensation of dopamine with 4-hydroxyphenylacetaldehyde is catalyzed by NCS to yield S-norcocIaurene, the central precursor of thousands of benzylisoquinoline alkaloids, including morphine. This poorly characterized, but key enzyme in benzylisoquinoline alkaloid biosynthesis has recently been purified to homogeneity, and its kinetic properties have been elucidated.35 NCS occurs as a 28 kDa dimer composed of 15 kDa... 

Second, while dopamine acts primarily at two receptor types, both of which produce slow potentials via G-protein-coupled mechanisms (i.e., metabotropic), glutamate mediates its effects at multiple postsynaptic receptors. While some glutamate receptors are metabotropic, the vast majority are coupled directly to ion channels (ionotropic). Different subtypes of glutamate receptors have different kinetic properties. 

Hemmings HC, Jr, Nairn AC, Greengard P (1984a) DARPP-32, a dopamine- and adenosine 3 5 -monophosphate-regulated neuronal phosphoprotein. II. Comparison of the kinetics of phosphorylation of DARPP-32 and phosphatase inhibitor 1. J Biol Chem 259 14491-14497. 

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