Dopamine measurement

Freeman A., Morales J., Beck J. et al. (2006). In vivo diurnal rhythm of dopamine measured in the putamen of non-human primates. Sleep 29(Abstr. Suppl.), A69. 

Smith GS, Dewey SL, Brodie JD, et al. Serotonergic modulation of dopamine measured with [ CJraclopride and PET in normal human subjects. Am J Psychiatry 1997 154 490-496. 

Bradberry, Charles W., Rand J. Gruen, Craig W. Berridge, and Robert H. Roth. 1991. "Individual Differences in Behavioral Measures Correlations with Nucleus Accumbens Dopamine Measured by Microdialysis." Pharmacology... 

Place on ice for 10 min followed by bench centrifuge (12,000-14,OOOg) for 5 min at 4°C. Transfer the clear supernatants to new, appropriately labelled tubes and store at -70°C until used for dopamine measurement. Dilution factor =10. 

Smith GS, Schloesser R, Brodie JD, Dewey SL, Logan J, et al. 1998. Glutamate modulation of dopamine measured in vivo with positron emission tomography (PET) and 11C-raclopride in normal human subjects. Neuropsychopharmacology 18 18-25. 

What is the actual concentration of dopamine at the dopamine receptors associated with each mode of firing of the dopamine cells The tonic level of dopamine measured using dialysis is 6.5 nM (Sam and Justice, 1996), consistent with predictions that the spatially averaged concentration of extracellular dopamine in the striatum is in the low nanomolar range (Kawagoe et ah, 1992). 

In an attempt to improve the selectivity of local dopamine measurements in the complex extracellular matrix of brain fluid, an implantable enzyme-based dopamine microbiosensor has been constructed based on the immobilization of tyrosinase in a thin-film chitosan coating of carbon-fiber disc microelectrodes [357]. o-Dopaquinone, which is the product of the tyrosinase reaction with dopamine, was monitored via its reduction at the modified microelectrode surface. The application of these cathodic tyrosinase dopamine microbiosensors was reported for the continuous real-time in vivo visualization of electrically stimulated dopamine release in the brain of anesthetized laboratory rats. Remarkably, due to the cathodic potential the sensor response was not significantly disturbed by the presence of typical interferences such as ascorbic and uric acid, serotonin, norepinephrine, and epinephrine. 

Application of the CCM to small sets (n < 6) of enzyme inhibitors revealed correlations between the inhibitory activity and the chirality measure of the inhibitors, calculated by Eq. (26) for the entire structure or for the substructure that interacts with the enzyme (pharmacophore) [41], This was done for arylammonium inhibitors of trypsin, Di-dopamine receptor inhibitors, and organophosphate inhibitors of trypsin, acetylcholine esterase, and butyrylcholine esterase. Because the CCM values are equal for opposite enantiomers, the method had to be applied separately to the two families of enantiomers (R- and S-enantiomers). 

Malison RT, Best SE, van Dyck CH, et al Elevated striatal dopamine transporters during acute cocaine abstinence as measured by [1231] beta-CIT SPECT. Am J... 

Dr. Gibb s hypothesis regarding dopamine involvement, we thought that perhaps MBDB would not be neurotoxic because of a lack of effect on dopamine. But, in fact, it is neurotoxic as well, measured by whole-brain serotonin 5-HIAA and tritiated paroxetine binding sites. It is perhaps two-thirds the toxicity, on a molecular weight basis, of MDMA, but it is toxic. 

In an attempt to simulate in rats the dosage regimen commonly employed by abusers of amphetamines, METH was administered (10 or 15 mg/kg every 6 hours four to six doses), after which the animals were killed (Koda and Gibb 1971 Koda and Gibb 1973). TH activity and catecholamine con-eentrations were measured in various brain regions and in the adrenal. Neostriatal TH aetivity was depressed in a dose-dependent manner and reaehed its nadir at 36 hours. Dopamine (DA) and norepinephrine concentrations were initially elevated, but then deereased in parallel with TH aetivity. Adrenal TH aetivity was elevated, presumably because of stress assoeiated with the toxie doses of METH. 

There are several ways in which possible neurotoxic effects might be studied. First, measurement of cerebrospinal fluid concentrations of dopamine or serotonin metabolites would be a straightforward way of assessing neurotoxicity. There are pitfalls in this approach (as outlined by Dr. Ricaurte (this volume), such as the facts that lumbar cerebrospinal fluid might reflect spinal cord neurochemistry more than it reflected brain neurochemistry, and drugs like /r-chloroamphetamine affect serotonin neurons in spinal cord less than they do those in brain (Sanders-Bush... 

A second approach might be to measure dopamine and serotonin along with their metabolites and other specific neuronal constituents such as tyrosine hydroxylase and tryptophan hydroxylase or uptake carrier sites in brain tissue obtained at autopsy. Accumulating data in this way might be a slow and tedious process, and drug dosing history might be uncertain and variable nonetheless, the approach deserves consideration. 

A third approach would be to measure some indicator of functional output of dopamine and/or serotonin neurons. As mentioned previously, studies in laboratory animals can be invaluable in defining parameters that change in correlation with directly measurable neurotoxic effects in the brain. 

Male Sprague-Dawl ey rats (200 -300 gm) were used in all experiments. Dopamine uptake was measured using the accumulation of tritium into a striatal synaptosomal fraction in the presence of an MAO inhibitor following a 5-minute incubation period with 10 nM 3H-DA at 37 °C. Uptake at 2 °C was used as a control for uptake by diffusion and was subtracted from uptake at 37 °C. 

Therapeutic measures that have been used to decrease the incidence of contrast-induced nephropathy include extracellular volume expansion, minimization of the amount of contrast administered, and treatment with oral acetylcysteine. Theophylline, fenoldopam, loop diuretics, mannitol, dopamine, and calcium antagonists have no effect or may worsen ARF. 

Insight into the state of dopaminergic tone is best obtained from measurements of extracellular dopamine in microdialysate samples collected from the behaving organism. Striatal (Paulson and Robinson 1994 Smith et al. 1992 Castaneda et al. 2004) and prefrontal cortical (Feenstra et al. 2000) dopamine levels rise in anticipation of, and are maintained throughout, the major wakefulness period in the rat, in concert with declines in dopamine metabolites (i.e., DOPAC, HVA, and 5-HIAA) (Smith et al. 1992 Whittaker et al. 1997). This pattern is... 

Hagan M. M., Havel P. J., Seeley R. J. et al (1999). Cerebrospinal fluid and plasma leptin measurements covariability with dopamine and cortisol in fasting humans. J. Clin. Endocrinol. Metah. 84(10), 3579-85. 

Hernandez, L., Auerbach, S., and Hoebel, B.G., Phencyclidine (PCP) injected into the nucleus accum-bens increases extracellular dopamine and serotonin as measured by microdialysis, Life Sci., 42, 1713, 1988. 

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