In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone
Identifieur interne : 001418 ( Main/Exploration ); précédent : 001417; suivant : 001419In vivo voltammetric studies on release mechanisms for cocaine with γ-butyrolactone
Auteurs : Patricia A. Broderick [États-Unis]Source :
- Pharmacology, Biochemistry and Behavior [ 0091-3057 ] ; 1991.
English descriptors
- Teeft :
- Accumbens, Accumbens synaptic concentrations, Animal control values, Anova, Basal, Baseline values, Brain dopamine, Broderick, Cocaine, Cocaine administration, Cocaine effects, Differential effects, Dopamine, Dopamine metabolites, Electrochemical, Experimental studies, Extracellular dopamine, Impulse flow, Impulse flow block, Impulse flow inhibition, Impulse flow inhibitor, Levels postmortem, Neuron, Neuronal, Neuronal impulse flow, Nucleus accumbens, Pharmacol, Presynaptic, Presynaptic mechanisms, Release mechanism, Release mechanisms, Reuptake inhibition, Rhesus monkeys, Same animal control, Serotonin, Spike discharges, Surgical procedure, Synaptic, Synaptic concentrations, Synaptie concentrations, Unrestrained, Uptake inhibition, Vivo, Vivo electrochemical, Vivo electrochemical signal, Vivo electrochemical signals, Vivo voltammetric, Vivo voltammetric studies, Vivo voltammetry, Voltammetric.
Abstract
Abstract: The effect of cocaine (20 mg/kg SC) on presynaptic mechanisms of release for dopamine (DA) and for serotonin (5-HT) was studied in nucleus accumbens of unrestrained rats (Rattus norvegicus). The studies were done by assaying synaptic concentrations of DA and 5-HT in the presence of the neuronal impulse flow inhibitor, γ-butyrolactone (γ-BL). The results were compared with cocaine effects on accumbens DA and 5-HT in the freely moving rat, without γ-BL treatment. A neurochemical time course profile showed that the cocaine-induced increase in accumbens synaptic concentrations of DA was significantly blocked (p<0.0001) after DA impulse flow was significantly inhibited (p<0.0038) by γ-BL (35.8%). The neurochemical time course profile concurrently showed that the cocaine-induced decrease in accumbens synaptic concentrations of 5-HT was significantly blocked (p<0.0004) after impulse flow was significantly inhibited (p<0.025) by γ-BL (50.6%). The findings show that cocaine's effects on synaptic concentrations for DA and for HT in accumbens are dependent on neuronal impulse flow. The findings indicate that presynaptic releasing mechanisms, which may be different for DA vis-à-vis 5-HT, play a role in the mechanism of action of cocaine.
Url:
DOI: 10.1016/0091-3057(91)90113-G
Affiliations:
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Broderick</name><affiliation wicri:level="1"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmacology, Room J-910, The City University of New York Medical School</wicri:regionArea><wicri:noRegion>The City University of New York Medical School</wicri:noRegion></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Biology and Psychology, CUNY Graduate School, Convent Ave.and W. 138th St., New York, NY 10031</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Pharmacology, Biochemistry and Behavior</title><title level="j" type="abbrev">PBB</title><idno type="ISSN">0091-3057</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1991">1991</date><biblScope unit="volume">40</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="969">969</biblScope><biblScope unit="page" to="975">975</biblScope></imprint><idno type="ISSN">0091-3057</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0091-3057</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Accumbens</term><term>Accumbens synaptic concentrations</term><term>Animal control values</term><term>Anova</term><term>Basal</term><term>Baseline values</term><term>Brain dopamine</term><term>Broderick</term><term>Cocaine</term><term>Cocaine administration</term><term>Cocaine effects</term><term>Differential effects</term><term>Dopamine</term><term>Dopamine metabolites</term><term>Electrochemical</term><term>Experimental studies</term><term>Extracellular dopamine</term><term>Impulse flow</term><term>Impulse flow block</term><term>Impulse flow inhibition</term><term>Impulse flow inhibitor</term><term>Levels postmortem</term><term>Neuron</term><term>Neuronal</term><term>Neuronal impulse flow</term><term>Nucleus accumbens</term><term>Pharmacol</term><term>Presynaptic</term><term>Presynaptic mechanisms</term><term>Release mechanism</term><term>Release mechanisms</term><term>Reuptake inhibition</term><term>Rhesus monkeys</term><term>Same animal control</term><term>Serotonin</term><term>Spike discharges</term><term>Surgical procedure</term><term>Synaptic</term><term>Synaptic concentrations</term><term>Synaptie concentrations</term><term>Unrestrained</term><term>Uptake inhibition</term><term>Vivo</term><term>Vivo electrochemical</term><term>Vivo electrochemical signal</term><term>Vivo electrochemical signals</term><term>Vivo voltammetric</term><term>Vivo voltammetric studies</term><term>Vivo voltammetry</term><term>Voltammetric</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The effect of cocaine (20 mg/kg SC) on presynaptic mechanisms of release for dopamine (DA) and for serotonin (5-HT) was studied in nucleus accumbens of unrestrained rats (Rattus norvegicus). The studies were done by assaying synaptic concentrations of DA and 5-HT in the presence of the neuronal impulse flow inhibitor, γ-butyrolactone (γ-BL). The results were compared with cocaine effects on accumbens DA and 5-HT in the freely moving rat, without γ-BL treatment. A neurochemical time course profile showed that the cocaine-induced increase in accumbens synaptic concentrations of DA was significantly blocked (p<0.0001) after DA impulse flow was significantly inhibited (p<0.0038) by γ-BL (35.8%). The neurochemical time course profile concurrently showed that the cocaine-induced decrease in accumbens synaptic concentrations of 5-HT was significantly blocked (p<0.0004) after impulse flow was significantly inhibited (p<0.025) by γ-BL (50.6%). The findings show that cocaine's effects on synaptic concentrations for DA and for HT in accumbens are dependent on neuronal impulse flow. The findings indicate that presynaptic releasing mechanisms, which may be different for DA vis-à-vis 5-HT, play a role in the mechanism of action of cocaine.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><noRegion><name sortKey="Broderick, Patricia A" sort="Broderick, Patricia A" uniqKey="Broderick P" first="Patricia A." last="Broderick">Patricia A. Broderick</name></noRegion><name sortKey="Broderick, Patricia A" sort="Broderick, Patricia A" uniqKey="Broderick P" first="Patricia A." last="Broderick">Patricia A. Broderick</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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