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A G Ewing

Publications and source records attributed to A G Ewing.

68 records · Page 4Linked to original sources
PubMed1988

Retention of ionic and non-ionic catechols in capillary zone electrophoresis with micellar solutions.

The use of micellar solutions in capillary zone electrophoresis has been primarily relegated to separations of non-ionic solutes, while its applicability to cationic species has been unexplored. We have found that the use of sodium dodecyl sulfate micelles in phosphate buffer allows for tremendous gains in selectivity for several cationic and non-ionic catechols over what can be obtained with normal capillary zone electrophoresis. Complexation of catechols with boric acid alters the net charge on the solutes and changes the partitioning behavior to produce adequate selectivity with improved analysis times. Although the mechanisms of solute interaction with the micellar phase for the cationic species are not decisively known, evidence is presented supporting the existence of ion-pairing equilibria simultaneously accompanied by micellar solubilization.

Borates↗
PubMed1985

Amphetamine attenuates the stimulated release of dopamine in vivo.

Carbon-fiber voltammetric electrodes have been used to measure the release of dopamine in the caudate nucleus of an anesthetized rat. Release is induced by electrical stimulation of the medial forebrain bundle. The amplitude of the observed release is attenuated by i.p. injection of amphetamine. A similar attenuation is induced by reserpine; however, at a slower rate. The combined regimen of amphetamine (1 or 10 mg/kg) and electrical stimulation does not deplete striatal dopamine levels and thus the decreased release of dopamine is not a result of depleted dopamine stores. Benztropine (25 mg kg-1) is able to cause a short term inhibition of the action of amphetamine (1 mg kg-1). The dopamine agonist pergolide (0.5 mg kg-1) does not affect the stimulated release. Haloperidol (1.0 mg kg-1) increases the amount of DA release, but is unable to attenuate the inhibition caused by amphetamine. Thus, it appears that the actions induced by amphetamine are a result of interaction with the neuronal uptake carrier and subsequent transport of dopamine from a functional to nonfunctional pool. In isolated striatal synaptic vesicles, amphetamine is found to block dopamine uptake and induce its release. This in vitro evidence provides a possible mechanism for the observed in vivo actions of amphetamine.

Animals↗
PubMed1984

In vitro comparison of the selectivity of electrodes for in vivo electrochemistry.

The properties of 4 types of carbon electrodes designed for use as in vivo sensors of easily oxidized species in the mammalian brain have been evaluated in aqueous solutions at physiological pH. The electrodes are formed from a graphite-epoxy mixture, carbon paste, or carbon fibers, and have the geometries of a disk or a cylinder. The voltammetric properties of several catecholamines, some of their metabolites and precursors, uric acid, and ascorbic acid are reported at unmodified carbon surfaces. The problem of overlap of the voltammetric waves of ascorbate and catechols is addressed, and two different methods which minimize this problem are examined. These are the use of disk-shaped electrodes fabricated from carbon fibers, which facilitate the use of subtracted voltammograms to determine small changes in the concentration of catecholamines in the presence of ascorbic acid, and the use of electrochemically modified, cylindrically-shaped electrodes also fabricated from carbon fibers. Voltammetry at the modified electrodes gives evidence the catechols can be resolved from ascorbate, and that catechols, but not ascorbic acid, adsorb to the electrode surface.

Animals↗
PubMed1984

Monitoring the stimulated release of dopamine with in vivo voltammetry. I: Characterization of the response observed in the caudate nucleus of the rat.

Microvoltammetric electrodes were employed in the brain of an anesthetized rat to monitor chemical substances in extracellular fluid following electrical stimulation of the medial forebrain bundle. An increase in concentration of an easily oxidized substance is observed in the caudate nucleus and in the nucleus accumbens. A large amount of evidence suggests that the substance that is observed following stimulation is dopamine. (1) The location of the stimulating electrode must be in known dopaminergic tracts to induce release. (2) Release is most easily observed in brain regions that contain significant numbers of dopamine-containing neurons. (3) Two voltammetric electrodes with very different electrochemical responses provide voltammograms of the released species that are unique for catechols in one case and catecholamines in another case. (4) The amount of 3,4-dihydroxyphenylacetic acid found in striatal tissue by postmortem analysis correlates with the calculated amount of dopamine released. (5) Inhibition of tyrosine hydroxylase, and thus dopamine synthesis, decreases the observed release while inhibition of monoamine oxidase, and thus formation of dopamine metabolites, does not. (6) The dependence of release on stimulation parameters agrees with results obtained with perfusion techniques. Thus, a new method has been developed to characterize endogenous dopamine release in the rat brain and can be used on a time scale of seconds.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Monitoring the stimulated release of dopamine with in vivo voltammetry. II: Clearance of released dopamine from extracellular fluid.

Microvoltammetric electrodes implanted in the caudate nucleus of the anesthetized rat have been used to monitor dopamine released following electrical stimulation of the medial forebrain bundle. These electrodes are fabricated from unmodified carbon fibers and have been used with normal pulse voltammetry. Dopamine appears in the vicinity of the electrode when the stimulation is initiated, and disappears almost immediately when the stimulation is terminated. The data suggest that the effective diffusion distance is less than 100 micron. Postmortem analysis using liquid chromatography with electrochemical detection shows that dopamine released in this manner is metabolized to 3,4-dihydroxyphenylacetic acid (DOPAC); however, neither substance is observed electrochemically in the extracellular fluid within seconds after the stimulation. In addition, inhibitors of neuronal uptake of dopamine, amphetamine (1.8 or 15 mg X kg-1) or benztropine (25 mg X kg-1), or of dopamine metabolism, pargyline (150 mg X kg-1) or tropolone (100 mg X kg-1), do not significantly affect the rate at which dopamine disappears from extracellular fluid, although they can affect the amount released. These results suggest that dopamine cannot freely diffuse in the extracellular fluid because an extraneuronal uptake mechanism exists that clears dopamine from extracellular fluid into an extraneuronal pool where metabolism to 3,4-dihydroxyphenylacetic acid occurs. Dopamine can be observed during electrical stimulation of the ascending fibers because neuronal and extraneuronal uptake systems are unable to remove dopamine on these short time scales.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Direct in vivo monitoring of dopamine released from two striatal compartments in the rat.

Microvoltammetric electrodes were used to monitor dopamine released in the caudate nucleus of the rat after electrical stimulation of the medial forebrain bundle. The time resolution of the technique is sufficient to determine in vivo concentration changes on a time scale of seconds. Direct evidence identifying the substance released as dopamine was obtained both voltammetrically and pharmacologically. Administration of alpha-methyl-p-tyrosine terminates the release of dopamine, although tissue stores of dopamine are still present. Thus there appears to be a compartment for dopamine storage that is not available for immediate release. This compartment appears to be mobilized by amfonelic acid, since administration of this agent after alpha-methyl-p-tyrosine returns the concentration of dopamine released by electrical stimulation to 75 percent of the original amount.

Amphetamine↗
PubMed1982

In vivo voltammetry with electrodes that discriminate between dopamine and ascorbate.

Untreated carbon-fiber voltammetric electrodes have been employed as chemical sensors of easily oxidized compounds in the brains of rats anesthetized with chloral hydrate. These electrodes can be used to distinguish dopamine from ascorbate and dihydroxyphenylacetate by the shape of the voltammograms. The electrodes are shown to provide a reproducible response to different neuronal stimuli. The rapid release of dopamine in the caudate nucleus can be measured following a local application of potassium chloride. Intraperitoneal injections of amphetamine also induce an increase of easily oxidized compounds; however, the voltammetry suggests that ascorbic acid, rather than dopamine, is the primary substance detected. Measurements in the cortex or in the caudate nucleus of animals lesioned by prior injection of 6-hydroxydopamine show that a substance with voltammetric properties identical to those of ascorbic acid also increases in concentration in these areas as a result of amphetamine administration.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

Evaluation of amphetamine-induced in vivo electrochemical response.

A carbon fiber microelectrode is shown to give a potential-dependent dopamine-selective response in rat brain tissue. However, distinct evidence for dopamine release is not obtained with intraperitoneal amphetamine administration (1.8 or 3.7 mg . kg-1). In rats which have been unilaterally depleted of dopamine, the change in electrochemical signal obtained in the lesioned striatum is very similar to that measured on the non-lesioned side following amphetamine administration. This indicates that substances other than dopamine contribute to the observed signals.

Amphetamine↗