Distinguishing effects of cocaine IV and SC on mesoaccumbens dopamine and serotonin release with chloral hydrate anesthesia
Identifieur interne : 000800 ( Istex/Corpus ); précédent : 000799; suivant : 000801Distinguishing effects of cocaine IV and SC on mesoaccumbens dopamine and serotonin release with chloral hydrate anesthesia
Auteurs : Patricia A. BroderickSource :
- Pharmacology, Biochemistry and Behavior [ 0091-3057 ] ; 1992.
English descriptors
- Teeft :
- Accumbens, Anesthesia, Anesthetic, Anova, Anova statistics, Ascorbic acid, Basal, Basal synaptic concentrations, Behav, Biochem, Brain power, Brain tissue, Broderick, Chloral, Chloral hydrate, Chloral hydrate anesthesia, Chloral paradigm, Cocaine, Cocaine administration, Cocaine effects, Daergic, Daergic response, Dopamine, Dopaminergic neurons, Electroactive, Electroactive species, Electrochemical, Electrochemical signal, Extracellular, General anesthetic effects, General anesthetics, Hydrate, Impulse flow, Mesoaccumbens, Microelectrode, Microelectrodes, Nacc, Neuroanatomic substrate, Neuron, Neuronal, Nucleus accumbens, Other hand, Pearson product, Pharmacol, Plsd, Posthoc, Posthoc analysis, Present data, Release mechanisms, Serotonin, Significant differences, Statistical significance, Synaptic, Synaptic concentrations, Temporal effects, Time period, Ventral, Ventral tegmental area, Ventrolateral nacc, Vivo, Vivo electrochemical signal, Vivo electrochemistry, Vivo voltammetric studies.
Abstract
Abstract: The effect of IV cocaine (0.5 and 1.0 mg/kg) was studied on synaptic concentrations of dopamine (DA) and serotonin [5-hydroxytryptamine (5-HT)] in the mesoaccumbens nerve terminal, the nucleus accumbens (NAcc), in chloral hydrate-anesthetized, male Sprague-Dawley rats (Rattus norvegicus) with in vivo electrochemistry (voltammetry). In further in vivo voltammetric studies, the effects of SC cocaine on synaptic concentrations of DA and 5-HT were studied in the chloral hydrate-anesthetized paradigm in two neuroanatomic substrates, NAcc and mesoaccumbens somatodendrites, the ventral tegmental area (VTA-A10), in a dose-response fashion (10, 20 and 40 mg/kg) in six separate studies. Moreover, in two additional in vivo voltammetric studies, again using the chloral hydrate-anesthetized paradigm, the impulse flow blocker, γ-butyrolactone (γ-BL) (750 mg/kg, IP), was studied alone and in combination with SC cocaine (20 mg/kg) to determine whether or not cocaine can act by presynaptic releasing mechanisms for DA and 5-HT. The results show that IV cocaine concurrently and significantly increased DA and 5-HT release in the NAcc (p < 0.001, p < 0.0005, respectively) at both doses tested. Moreover, IV cocaine effects on DA and 5-HT release were significantly and positively correlated (p < 0.01). On the other hand, SC cocaine concurrently and significantly decreased DA and 5-HT release in NAcc (p < 0.0001) and VTA (p < 0.0001) at each separate dose tested. SC cocaine effects on DA and 5-HT release were significantly and positively correlated across dose and neuroanatomic substrate (p < 0.01). Furthermore, the γ-BL studies indicate that cocaine's action includes a presynaptic release mechanism for the biogenic amines. Summarily, the data show that a consideration of the route of cocaine administration is crucial in determining the underlying neurochemical basis for cocaine.
Url:
DOI: 10.1016/0091-3057(92)90427-H
Links to Exploration step
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<front><div type="abstract" xml:lang="en">Abstract: The effect of IV cocaine (0.5 and 1.0 mg/kg) was studied on synaptic concentrations of dopamine (DA) and serotonin [5-hydroxytryptamine (5-HT)] in the mesoaccumbens nerve terminal, the nucleus accumbens (NAcc), in chloral hydrate-anesthetized, male Sprague-Dawley rats (Rattus norvegicus) with in vivo electrochemistry (voltammetry). In further in vivo voltammetric studies, the effects of SC cocaine on synaptic concentrations of DA and 5-HT were studied in the chloral hydrate-anesthetized paradigm in two neuroanatomic substrates, NAcc and mesoaccumbens somatodendrites, the ventral tegmental area (VTA-A10), in a dose-response fashion (10, 20 and 40 mg/kg) in six separate studies. Moreover, in two additional in vivo voltammetric studies, again using the chloral hydrate-anesthetized paradigm, the impulse flow blocker, γ-butyrolactone (γ-BL) (750 mg/kg, IP), was studied alone and in combination with SC cocaine (20 mg/kg) to determine whether or not cocaine can act by presynaptic releasing mechanisms for DA and 5-HT. The results show that IV cocaine concurrently and significantly increased DA and 5-HT release in the NAcc (p < 0.001, p < 0.0005, respectively) at both doses tested. Moreover, IV cocaine effects on DA and 5-HT release were significantly and positively correlated (p < 0.01). On the other hand, SC cocaine concurrently and significantly decreased DA and 5-HT release in NAcc (p < 0.0001) and VTA (p < 0.0001) at each separate dose tested. SC cocaine effects on DA and 5-HT release were significantly and positively correlated across dose and neuroanatomic substrate (p < 0.01). Furthermore, the γ-BL studies indicate that cocaine's action includes a presynaptic release mechanism for the biogenic amines. Summarily, the data show that a consideration of the route of cocaine administration is crucial in determining the underlying neurochemical basis for cocaine.</div>
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<abstract>Abstract: The effect of IV cocaine (0.5 and 1.0 mg/kg) was studied on synaptic concentrations of dopamine (DA) and serotonin [5-hydroxytryptamine (5-HT)] in the mesoaccumbens nerve terminal, the nucleus accumbens (NAcc), in chloral hydrate-anesthetized, male Sprague-Dawley rats (Rattus norvegicus) with in vivo electrochemistry (voltammetry). In further in vivo voltammetric studies, the effects of SC cocaine on synaptic concentrations of DA and 5-HT were studied in the chloral hydrate-anesthetized paradigm in two neuroanatomic substrates, NAcc and mesoaccumbens somatodendrites, the ventral tegmental area (VTA-A10), in a dose-response fashion (10, 20 and 40 mg/kg) in six separate studies. Moreover, in two additional in vivo voltammetric studies, again using the chloral hydrate-anesthetized paradigm, the impulse flow blocker, γ-butyrolactone (γ-BL) (750 mg/kg, IP), was studied alone and in combination with SC cocaine (20 mg/kg) to determine whether or not cocaine can act by presynaptic releasing mechanisms for DA and 5-HT. The results show that IV cocaine concurrently and significantly increased DA and 5-HT release in the NAcc (p > 0.001, p > 0.0005, respectively) at both doses tested. Moreover, IV cocaine effects on DA and 5-HT release were significantly and positively correlated (p > 0.01). On the other hand, SC cocaine concurrently and significantly decreased DA and 5-HT release in NAcc (p > 0.0001) and VTA (p > 0.0001) at each separate dose tested. SC cocaine effects on DA and 5-HT release were significantly and positively correlated across dose and neuroanatomic substrate (p > 0.01). Furthermore, the γ-BL studies indicate that cocaine's action includes a presynaptic release mechanism for the biogenic amines. Summarily, the data show that a consideration of the route of cocaine administration is crucial in determining the underlying neurochemical basis for cocaine.</abstract>
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<abstract xml:lang="en"><p>Abstract: The effect of IV cocaine (0.5 and 1.0 mg/kg) was studied on synaptic concentrations of dopamine (DA) and serotonin [5-hydroxytryptamine (5-HT)] in the mesoaccumbens nerve terminal, the nucleus accumbens (NAcc), in chloral hydrate-anesthetized, male Sprague-Dawley rats (Rattus norvegicus) with in vivo electrochemistry (voltammetry). In further in vivo voltammetric studies, the effects of SC cocaine on synaptic concentrations of DA and 5-HT were studied in the chloral hydrate-anesthetized paradigm in two neuroanatomic substrates, NAcc and mesoaccumbens somatodendrites, the ventral tegmental area (VTA-A10), in a dose-response fashion (10, 20 and 40 mg/kg) in six separate studies. Moreover, in two additional in vivo voltammetric studies, again using the chloral hydrate-anesthetized paradigm, the impulse flow blocker, γ-butyrolactone (γ-BL) (750 mg/kg, IP), was studied alone and in combination with SC cocaine (20 mg/kg) to determine whether or not cocaine can act by presynaptic releasing mechanisms for DA and 5-HT. The results show that IV cocaine concurrently and significantly increased DA and 5-HT release in the NAcc (p < 0.001, p < 0.0005, respectively) at both doses tested. Moreover, IV cocaine effects on DA and 5-HT release were significantly and positively correlated (p < 0.01). On the other hand, SC cocaine concurrently and significantly decreased DA and 5-HT release in NAcc (p < 0.0001) and VTA (p < 0.0001) at each separate dose tested. SC cocaine effects on DA and 5-HT release were significantly and positively correlated across dose and neuroanatomic substrate (p < 0.01). Furthermore, the γ-BL studies indicate that cocaine's action includes a presynaptic release mechanism for the biogenic amines. Summarily, the data show that a consideration of the route of cocaine administration is crucial in determining the underlying neurochemical basis for cocaine.</p>
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<textClass><keywords scheme="keyword"><list><head>Keywords</head>
<item><term>Cocaine</term>
</item>
<item><term>Dopamine</term>
</item>
<item><term>Serotonin</term>
</item>
<item><term>Ventrolateral nucleus accumbens</term>
</item>
<item><term>In vivo electrochemistry (voltammetry)</term>
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<item><term>Chloral hydrate anesthesia</term>
</item>
<item><term>Ventral tegmental area</term>
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<head><ce:dochead><ce:textfn>Rapid communication</ce:textfn>
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<ce:title>Distinguishing effects of cocaine IV and SC on mesoaccumbens dopamine and serotonin release with chloral hydrate anesthesia</ce:title>
<ce:author-group><ce:author><ce:given-name>Patricia A.</ce:given-name>
<ce:surname>Broderick</ce:surname>
<ce:cross-ref refid="COR1"><ce:sup>1</ce:sup>
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<ce:affiliation id="AFF1"><ce:label>a</ce:label>
<ce:textfn>Department of Pharmacology, The City University of New York Medical School, USA</ce:textfn>
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<ce:affiliation id="AFF2"><ce:label>b</ce:label>
<ce:textfn>Departments of Biology and Psychology, CUNY Graduate School, New York, NY 10031, USA</ce:textfn>
</ce:affiliation>
<ce:correspondence id="COR1"><ce:label>1</ce:label>
<ce:text>Requests for reprints should be addressed to Dr. Patricia A. Broderick, Department of Pharmacology, Room J-910, The City University of New York Medical School, and Departments of Biology and Psychology, CUNY Graduate School, Convent Avenue and West 138th Street, New York, NY 10031, USA.</ce:text>
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<ce:date-received day="24" month="6" year="1992"></ce:date-received>
<ce:abstract><ce:section-title>Abstract</ce:section-title>
<ce:abstract-sec><ce:simple-para>The effect of IV cocaine (0.5 and 1.0 mg/kg) was studied on synaptic concentrations of dopamine (DA) and serotonin [5-hydroxytryptamine (5-HT)] in the mesoaccumbens nerve terminal, the nucleus accumbens (NAcc), in chloral hydrate-anesthetized, male Sprague-Dawley rats (<ce:italic>Rattus norvegicus</ce:italic>
) with in vivo electrochemistry (voltammetry). In further in vivo voltammetric studies, the effects of SC cocaine on synaptic concentrations of DA and 5-HT were studied in the chloral hydrate-anesthetized paradigm in two neuroanatomic substrates, NAcc and mesoaccumbens somatodendrites, the ventral tegmental area (VTA-A<ce:inf>10</ce:inf>
), in a dose-response fashion (10, 20 and 40 mg/kg) in six separate studies. Moreover, in two additional in vivo voltammetric studies, again using the chloral hydrate-anesthetized paradigm, the impulse flow blocker, γ-butyrolactone (γ-BL) (750 mg/kg, IP), was studied alone and in combination with SC cocaine (20 mg/kg) to determine whether or not cocaine can act by presynaptic releasing mechanisms for DA and 5-HT. The results show that IV cocaine concurrently and significantly increased DA and 5-HT release in the NAcc (<ce:italic>p</ce:italic>
< 0.001, <ce:italic>p</ce:italic>
< 0.0005, respectively) at both doses tested. Moreover, IV cocaine effects on DA and 5-HT release were significantly and positively correlated (<ce:italic>p</ce:italic>
< 0.01). On the other hand, SC cocaine concurrently and significantly decreased DA and 5-HT release in NAcc (<ce:italic>p</ce:italic>
< 0.0001) and VTA (<ce:italic>p</ce:italic>
< 0.0001) at each separate dose tested. SC cocaine effects on DA and 5-HT release were significantly and positively correlated across dose and neuroanatomic substrate (<ce:italic>p</ce:italic>
< 0.01). Furthermore, the γ-BL studies indicate that cocaine's action includes a presynaptic release mechanism for the biogenic amines. Summarily, the data show that a consideration of the route of cocaine administration is crucial in determining the underlying neurochemical basis for cocaine.</ce:simple-para>
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<ce:keywords><ce:section-title>Keywords</ce:section-title>
<ce:keyword><ce:text>Cocaine</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Dopamine</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Serotonin</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Ventrolateral nucleus accumbens</ce:text>
</ce:keyword>
<ce:keyword><ce:text>In vivo electrochemistry (voltammetry)</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Chloral hydrate anesthesia</ce:text>
</ce:keyword>
<ce:keyword><ce:text>Ventral tegmental area</ce:text>
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<affiliation>Department of Pharmacology, The City University of New York Medical School, USA</affiliation>
<description>Requests for reprints should be addressed to Dr. Patricia A. Broderick, Department of Pharmacology, Room J-910, The City University of New York Medical School, and Departments of Biology and Psychology, CUNY Graduate School, Convent Avenue and West 138th Street, New York, NY 10031, USA.</description>
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<abstract lang="en">Abstract: The effect of IV cocaine (0.5 and 1.0 mg/kg) was studied on synaptic concentrations of dopamine (DA) and serotonin [5-hydroxytryptamine (5-HT)] in the mesoaccumbens nerve terminal, the nucleus accumbens (NAcc), in chloral hydrate-anesthetized, male Sprague-Dawley rats (Rattus norvegicus) with in vivo electrochemistry (voltammetry). In further in vivo voltammetric studies, the effects of SC cocaine on synaptic concentrations of DA and 5-HT were studied in the chloral hydrate-anesthetized paradigm in two neuroanatomic substrates, NAcc and mesoaccumbens somatodendrites, the ventral tegmental area (VTA-A10), in a dose-response fashion (10, 20 and 40 mg/kg) in six separate studies. Moreover, in two additional in vivo voltammetric studies, again using the chloral hydrate-anesthetized paradigm, the impulse flow blocker, γ-butyrolactone (γ-BL) (750 mg/kg, IP), was studied alone and in combination with SC cocaine (20 mg/kg) to determine whether or not cocaine can act by presynaptic releasing mechanisms for DA and 5-HT. The results show that IV cocaine concurrently and significantly increased DA and 5-HT release in the NAcc (p < 0.001, p < 0.0005, respectively) at both doses tested. Moreover, IV cocaine effects on DA and 5-HT release were significantly and positively correlated (p < 0.01). On the other hand, SC cocaine concurrently and significantly decreased DA and 5-HT release in NAcc (p < 0.0001) and VTA (p < 0.0001) at each separate dose tested. SC cocaine effects on DA and 5-HT release were significantly and positively correlated across dose and neuroanatomic substrate (p < 0.01). Furthermore, the γ-BL studies indicate that cocaine's action includes a presynaptic release mechanism for the biogenic amines. Summarily, the data show that a consideration of the route of cocaine administration is crucial in determining the underlying neurochemical basis for cocaine.</abstract>
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<subject><genre>Keywords</genre>
<topic>Cocaine</topic>
<topic>Dopamine</topic>
<topic>Serotonin</topic>
<topic>Ventrolateral nucleus accumbens</topic>
<topic>In vivo electrochemistry (voltammetry)</topic>
<topic>Chloral hydrate anesthesia</topic>
<topic>Ventral tegmental area</topic>
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