In vitro and in vivo characterization of the properties of a multifiber carbon electrode allowing long-term electrochemical detection of dopamine in freely moving animals.
We recently developed a multifiber carbon electrode for voltammetric studies which shows an apparent selectivity for dopamine (DA) in vitro and which can be used over very long periods of time after implantation for in vivo recordings in the striatum of rodents. This series of experiments was undertaken to further characterize our voltammetric signal detected in the brain. Comparison of voltammetric signals obtained in vitro after electric pretreatment of the electrode in solutions of various oxidizable endogenous compounds at regularly increasing concentrations showed that the sensitivity of the electrode for DA is 10,000 times higher than for ascorbic acid (AA) and 1000 times higher than for 3,4-dihydroxyphenylacetic acid (DOPAC), two compounds which are detectable in vivo. Measurements of the DA signal in the presence of DOPAC or AA showed that interactions occurred between the oxidized forms of the various molecules. DOPAC decreased the DA sensitivity of the electrode, whereas a potentiation of the DA signal was observed with AA at high concentrations, showing the presence of an electro-catalytic effect. At lower AA concentrations a decreased DA sensitivity of the electrode was observed as in the case of DOPAC. The brain distribution of the in vivo voltammetric signal was studied in anesthetized hamsters, showing a regional specificity which was positively correlated to the dopaminergic innervation. In animals with chronically implanted electrodes, various pharmacological compounds known to interfere with DA metabolism or the activity of dopaminergic neurons were injected. alpha-Methyl-p-tyrosine and reserpine were shown to induce a decrease in signal amplitude. Similar data were obtained with gamma-hydroxybutyrate and gamma-butyrolactone, which have been previously shown to decrease the dopaminergic neuronal firing rate. An increase in the striatal response was on the contrary obtained in anesthetized rats following electrical stimulation of the medial forebrain bundle containing dopaminergic fibers. Drugs acting on dopaminergic receptors such as neuroleptics and apomorphine, were shown to increase and diminish the striatal signal, respectively. Finally, AA peripheral administration was found to reduce the striatal signal amplitude. These data reinforce the idea that DA mainly contributes to our in vivo brain voltammetric response, although extracellular DOPAC or AA levels may influence this response. Variations in the striatal voltammetric signal recorded in vivo in freely moving animals over very long periods of time after electrode implantation may thus reflect variations in the activity of the nigrostriatal dopaminergic neurons.
D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology; D001921:Brain / Q000378:metabolism*; D002244:Carbon; D002395:Catecholamines / Q000378:metabolism; D002697:Chloral Hydrate / Q000494:pharmacology; D006224:Cricetinae; D004298:Dopamine / Q000378:metabolism*; D004347:Drug Interactions; D004558:Electric Stimulation; D004563:Electrochemistry / Q000295:instrumentation / Q000379:methods*; D004566:Electrodes; D008474:Medial Forebrain Bundle / Q000502:physiology; D008647:Mesocricetus; D009068:Movement; D010084:Oxidation-Reduction; D011954:Receptors, Dopamine / Q000502:physiology; D014527:Uric Acid / Q000378:metabolism
D002395:Catecholamines; D011954:Receptors, Dopamine; D014527:Uric Acid; D002697:Chloral Hydrate; D002244:Carbon; D001205:Ascorbic Acid; D004298:Dopamine