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• W2015144460 startingPage "69" @default.
• W2015144460 abstract "Differential pulse voltammetry used in combination with an electrochemically treated carbon fiber electrode allowed to detect ascorbic acid (AA) and 3,4-dihydroxyphenylacetic acid (DOPAC) in the striatum of unanaesthetized freely moving rats. Carbon fiber electrodes were implanted under light halothane anaesthesia. When the rat recovered from anaesthesia, voltammograms were recorded every 2.5 min for about 5 h. During the last 3 h the signals corresponding to AA and DOPAC appeared stable and reproducible, allowing comparisons between control and pharmacological experiments. After the in vivo experiments, the electrodes were calibrated in AA and DOPAC solutions. Striatal AA and DOPAC levels were thus estimated to be 306 and 17.7 μM respectively. DOPAC signals were increased by haloperidol and chloral hydrate, decreased by amphetamine and suppressed by pargyline. In pargyline pretreated rats the catechol signal slightly re-appeared after amphetamine injections. This signal was attributed to dopamine (DA) and estimated to a concentration50NM DA. The AA current recorded in the striatum was not modified when dopaminergic terminals selectively degenerated. The AA signal was decreased by chloral hydrate or halothane anaesthesia and increased by amphetamine injections. This latter effect depended on the presence of dopaminergic terminals. This shows that the increasing current effect of amphetamine, previously observed by non-selective techniques, should be attributed to AA rather than DA. These results confirm that the catechol compound electrochemically detected in the striatum is the direct metabolite of the DA, i.e. DOPAC, and support the thesis of a functional relationship between AA levels and dopaminergic neurotransmission." @default.
• W2015144460 created "2016-06-24" @default.
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• W2015144460 date "1981-10-01" @default.
• W2015144460 modified "2023-10-10" @default.
• W2015144460 title "Voltammetry in the striatum of chronic freely moving rats: Detection of catechols and ascorbic acid" @default.
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• W2015144460 doi "https://doi.org/10.1016/0006-8993(81)90807-6" @default.
• W2015144460 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7284811" @default.
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