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J Cammack

Publications and source records attributed to J Cammack.

10 recordsLinked to original sources

Electrochemical monitoring of brain ascorbic acid changes associated with hypoxia, spreading depression, and seizure activity.

In vivo electrochemistry has been a valuable tool in detecting real time neurochemical changes in extracellular fluid. Absolute selectivity has been difficult to achieve previously, but we report here a carbon fiber electrode and measurement technique which is specific for one oxidizable species: ascorbic acid. Ascorbic acid is highly concentrated in extra- as well as intracellular brain spaces, and appears to undergo dynamic changes in response to a variety of physiological and pathophysiological circumstances. Recent studies have implicated glutamatergic mechanisms which give rise to extracellular changes in brain ascorbate, and we confirm and extend these observations. Preliminary studies, directed towards examining ascorbic acid as an index and/or result of hypoxia, spreading depression, and seizure activity, have been undertaken and the results are reported herein.

Animals↗

The pharmacological profile of glutamate-evoked ascorbic acid efflux measured by in vivo electrochemistry.

A recently described in vivo voltammetric electrode selectively records rapid changes in extracellular fluid (ECF) levels of ascorbic acid. Using this detector, the nature of glutamate-induced efflux of ascorbate into ECF was investigated using pharmacological tools. Ascorbate signals were shown to be directly related to amounts of microinjected glutamate. Blockers of glutamate reuptake, homocysteic acid and D,L-threo-beta-hydroxy-aspartic acid, virtually eliminate the ascorbate signal. A more specific reuptake blocker (the stilbene isothiocyano derivative (SITS) does not completely inhibit ascorbate efflux, suggesting that the glutamate uptake which is coupled to ascorbic acid exchange is both neuronal and glial in nature. Other pharmacological experiments indicate that excitatory amino acid receptors are not involved in the glutamate-elicited ascorbate efflux; it is primarily a function of the glutamate/ascorbate heteroexchange process as described earlier. The possible role(s) of brain ascorbate in the general functioning of the pervasive glutamate neurotransmitter systems are discussed.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

Anoxia-resistant turtle brain maintains ascorbic acid content in vitro.

The isolated turtle brain maintains intra- and extracellular concentrations of ascorbate when incubated in ascorbate-free physiological saline for as long as 24 h. After incubation for 1 h, total tissue content of ascorbate in the turtle cerebellum was the same as in unincubated controls. After 20-24 h, tissue ascorbate content remained at 65% of control levels, while extracellular ascorbate concentration, measured with carbon fiber voltammetric microelectrodes, was 56% of the initial value. For an intermediate incubation period of 6 h, reduced ascorbate content was maintained at about 80% of control levels, regardless of whether incubation was under normal conditions or in the absence of glucose or oxygen. By contrast, only 4% of the ascorbate content of guinea pig brain slices remained after a 6 h incubation. Maintenance of high levels of ascorbate by the anoxia-resistant turtle brain could be an important factor in the amelioration of oxidative injury in this tissue. Inclusion of ascorbate in media used for in vitro studies of mammalian brain tissue is recommended.

Animals↗

Antioxidants prevent the interaction of 3,4-dihydroxyphenylacetic acid at the dopamine D2 receptor.

Antioxidants such as ascorbic acid (AA) and dithiothreitol (DTT), can prevent 3,4-dihydroxyphenylacetic acid (DOPAC) inhibition of [3H]spiperone binding to neuronal dopamine D2 receptors. The DOPAC quinone produced from auto-oxidation is believed to be responsible for the irreversible inhibition noted. Quinone conjugation to proteins occurs readily in vivo, and thus, auto-oxidation of DOPAC and other endogenous catechol containing compounds could be an important component of protein modification during on-going neuronal physiology.

3,4-Dihydroxyphenylacetic Acid↗

Dynamic changes in extracellular fluid ascorbic acid monitored by in vivo electrochemistry.

Voltammetric carbon fiber electrodes and a measuring protocol were designed to monitor extracellular changes in rat brain ascorbic acid (AA). Very fast variations of AA (less than 60 s in duration) as well as much slower changes can be followed. Basal and stimulated levels of AA, determined with the enzyme ascorbate oxidase (AAO), confirm the detection is selective for AA. Microinjections of glutamate (Glu) into various brain regions gave rise to rapid electrochemical signals ascribed to the efflux of AA into the extracellular fluid.

Animals↗

Simultaneous high-performance liquid chromatographic determination of ascorbic acid and dehydroascorbic acid in biological samples.

The ascorbic acid (AA)-dehydroascorbic acid redox couple is an important component of many biological systems, and various physiological roles have been described for this vitamin. Simultaneous measurement of both AA and dehydroascorbate using high-performance liquid chromatography (HPLC) has proven difficult owing to detection problems. A simple, single-step HPLC assay for the simultaneous detection of both AA and dehydroascorbate was developed without the burden of derivatization of either compounds. This has proven to be a reliable technique and should be applicable to a wide variety of biological samples.

Animals↗

Psychological stress and the passage of a standard meal through the stomach and small intestine in man.

Gastric emptying half-time and mouth to caecum transit time of a solid meal were measured in eight normal volunteers, once during a period of psychological stress and again during a period of relative calm. No consistent or significant effect on gastric emptying was observed, but mouth to caecum transit times were faster in all subjects and this difference was highly significant (p<0.01).

Adult↗

Is the transit time of a meal through the small intestine related to the rate at which it leaves the stomach?

Using non-invasive techniques, we investigated how varying the size or composition of a meal altered the rate at which it passed through the stomach and small intestine in normal volunteers. Increasing the size of the meal by doubling the absorbable components delayed gastric emptying, did not significantly influence the time taken for the head of the meal to reach the caecum, but retarded the entry of the bulk of the meal residues into the caecum. Incorporating fat in the meal slowed gastric emptying, but did not significantly affect small bowel transit time. The addition of the unabsorbable disaccharide lactulose (in place of an equivalent amount of sucrose) accelerated small bowel transit time, but did not significantly influence gastric emptying. Thus, our results indicated that changes in small bowel transit time could occur independently of changes in gastric emptying in normal healthy subjects.

Adult↗

Effect of prolonged exercise on the passage of a solid meal through the stomach and small intestine.

The effect of intermittent moderate exercise on the passage of a solid meal, labelled with radioactive Technetium sulphur colloid, through the stomach and small intestine was investigated by paired studies on seven healthy volunteers. Measurements of gastric radioactivity and breath hydrogen exertion were recorded every 10 minutes while subjects exercised in a controlled manner while seated on a bicycle ergometer. These were compared with values obtained during a separate experiment while the same subjects sat upright in a chair. Exercise significantly accelerated gastric emptying (control t 1/2 = 1.5 +/- 0.1 h; exercise t 1/2 = 1.2 +/- 0.1 h; p less than 0.02) but had no significant effect on small bowel transit time.

Adult↗