Electrophysiological characterization of harmane-induced activation of mesolimbic dopamine neurons
Identifieur interne : 000597 ( PascalFrancis/Corpus ); précédent : 000596; suivant : 000598Electrophysiological characterization of harmane-induced activation of mesolimbic dopamine neurons
Auteurs : Ouafa Arib ; Pascal Rat ; Robert Molimard ; Abderrahman Chait ; Philippe Faure ; Renaud De BeaurepaireSource :
- European journal of pharmacology [ 0014-2999 ] ; 2010.
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Abstract
It has been suggested that the beta-carbolines harmane and norharmane may be involved in the pathophysiology of Parkinson's disease, psychosis and addiction, but the mechanisms of these possible effects remain to be elucidated. In the present study, the effects of the two compounds were examined by using in vivo extracellular recordings of ventral tegmental dopamine neurons. The effects of harmane (2 mg/kg) and norharmane (2 mg/kg), were compared to those of nicotine (11 μg/kg), of cotinine (0.5 mg/kg), of the monoamine-oxidase-A inhibitor befloxatone (0.12 mg/kg), and of the monoamine-oxidase-B inhibitor selegiline (0.5 mg/kg). The effects of harmane were also tested after pre-treatment with the nicotine receptor antagonist mecamylamine. The results show that all substances, except befloxatone, activate the firing and/or burst activity of dopamine neurons. The increase in firing rate produced by harmane was approximately 18 times greater than that produced by nicotine. Such powerful excitation of dopamine neurons by harmane may in part explain its involvement in neurotoxicity, psychosis and addiction. The absence of effect of befloxatone supports the hypothesis that the effect of harmane is not related to its monoamine-oxidase-A inhibitory properties. Mecamylamine inhibited by approximately 80% the activity of harmane, indicating that the activating effect of harmane on dopamine neurons involves several mechanisms, among which activation of nicotinic receptors likely has a prominent importance. The results of the present study support the hypothesis that harmane could be a tobacco (or smoke) component other than nicotine involved in tobacco dependence.
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Format Inist (serveur)
| NO : | PASCAL 10-0152691 INIST |
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| ET : | Electrophysiological characterization of harmane-induced activation of mesolimbic dopamine neurons |
| AU : | ARIB (Ouafa); RAT (Pascal); MOLIMARD (Robert); CHAIT (Abderrahman); FAURE (Philippe); DE BEAUREPAIRE (Renaud) |
| AF : | Laboratoire de Psychopharmacologie, Centre Hospitalier Paul Guiraud, 54 avenue de la Republique/94806 Villejuif/France (1 aut., 2 aut., 3 aut., 6 aut.); Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur/75724 Paris/France (1 aut., 5 aut.); Département de Biologie, Faculté Semlalia, Universit Cadi Ayyad/40 000 Marrakech/Maroc (4 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | European journal of pharmacology; ISSN 0014-2999; Coden EJPHAZ; Pays-Bas; Da. 2010; Vol. 629; No. 1-3; Pp. 47-52; Bibl. 1/4 p. |
| LA : | Anglais |
| EA : | It has been suggested that the beta-carbolines harmane and norharmane may be involved in the pathophysiology of Parkinson's disease, psychosis and addiction, but the mechanisms of these possible effects remain to be elucidated. In the present study, the effects of the two compounds were examined by using in vivo extracellular recordings of ventral tegmental dopamine neurons. The effects of harmane (2 mg/kg) and norharmane (2 mg/kg), were compared to those of nicotine (11 μg/kg), of cotinine (0.5 mg/kg), of the monoamine-oxidase-A inhibitor befloxatone (0.12 mg/kg), and of the monoamine-oxidase-B inhibitor selegiline (0.5 mg/kg). The effects of harmane were also tested after pre-treatment with the nicotine receptor antagonist mecamylamine. The results show that all substances, except befloxatone, activate the firing and/or burst activity of dopamine neurons. The increase in firing rate produced by harmane was approximately 18 times greater than that produced by nicotine. Such powerful excitation of dopamine neurons by harmane may in part explain its involvement in neurotoxicity, psychosis and addiction. The absence of effect of befloxatone supports the hypothesis that the effect of harmane is not related to its monoamine-oxidase-A inhibitory properties. Mecamylamine inhibited by approximately 80% the activity of harmane, indicating that the activating effect of harmane on dopamine neurons involves several mechanisms, among which activation of nicotinic receptors likely has a prominent importance. The results of the present study support the hypothesis that harmane could be a tobacco (or smoke) component other than nicotine involved in tobacco dependence. |
| CC : | 002B02B06; 002B17G; 002B03E; 002B17A01 |
| FD : | Electrophysiologie; Caractérisation; Neurone dopaminergique; Nicotine; Amine oxidase (flavin-containing); Sélégiline; Béfloxatone; Maladie de Parkinson; Psychose; Tabagisme; Antiparkinsonien; Psychotrope; Antidépresseur; Harmane dérivé; β-Carboline dérivé |
| FG : | Oxidoreductases; Enzyme; Alcaloïde; Inhibiteur de la monoamine oxidase B; Inhibiteur enzyme; Inhibiteur de la monoamine oxidase A; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Pathologie du système nerveux |
| ED : | Electrophysiology; Characterization; Dopaminergic neuron; Nicotine; Amine oxidase (flavin-containing); Selegiline; Befloxatone; Parkinson disease; Psychosis; Tobacco smoking; Antiparkinson agent; Psychotropic; Antidepressant agent |
| EG : | Oxidoreductases; Enzyme; Alkaloid; Monoamine oxidase B inhibitor; Enzyme inhibitor; Monoamine oxidase A inhibitor; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases |
| SD : | Electrofisiología; Caracterización; Neurona dopaminérgica; Nicotina; Amine oxidase (flavin-containing); Selegilina; Befloxatona; Parkinson enfermedad; Psicosis; Tabaquismo; Antiparkinsoniano; Psicotropo; Antidepresor |
| LO : | INIST-13322.354000190111890080 |
| ID : | 10-0152691 |
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when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">European journal of pharmacology</title><title level="j" type="abbreviated">Eur. j. pharmacol.</title><idno type="ISSN">0014-2999</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amine oxidase (flavin-containing)</term><term>Antidepressant agent</term><term>Antiparkinson agent</term><term>Befloxatone</term><term>Characterization</term><term>Dopaminergic neuron</term><term>Electrophysiology</term><term>Nicotine</term><term>Parkinson disease</term><term>Psychosis</term><term>Psychotropic</term><term>Selegiline</term><term>Tobacco smoking</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Electrophysiologie</term><term>Caractérisation</term><term>Neurone dopaminergique</term><term>Nicotine</term><term>Amine oxidase (flavin-containing)</term><term>Sélégiline</term><term>Béfloxatone</term><term>Maladie de Parkinson</term><term>Psychose</term><term>Tabagisme</term><term>Antiparkinsonien</term><term>Psychotrope</term><term>Antidépresseur</term><term>Harmane dérivé</term><term>β-Carboline dérivé</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">It has been suggested that the beta-carbolines harmane and norharmane may be involved in the pathophysiology of Parkinson's disease, psychosis and addiction, but the mechanisms of these possible effects remain to be elucidated. In the present study, the effects of the two compounds were examined by using in vivo extracellular recordings of ventral tegmental dopamine neurons. The effects of harmane (2 mg/kg) and norharmane (2 mg/kg), were compared to those of nicotine (11 μg/kg), of cotinine (0.5 mg/kg), of the monoamine-oxidase-A inhibitor befloxatone (0.12 mg/kg), and of the monoamine-oxidase-B inhibitor selegiline (0.5 mg/kg). The effects of harmane were also tested after pre-treatment with the nicotine receptor antagonist mecamylamine. The results show that all substances, except befloxatone, activate the firing and/or burst activity of dopamine neurons. The increase in firing rate produced by harmane was approximately 18 times greater than that produced by nicotine. Such powerful excitation of dopamine neurons by harmane may in part explain its involvement in neurotoxicity, psychosis and addiction. The absence of effect of befloxatone supports the hypothesis that the effect of harmane is not related to its monoamine-oxidase-A inhibitory properties. Mecamylamine inhibited by approximately 80% the activity of harmane, indicating that the activating effect of harmane on dopamine neurons involves several mechanisms, among which activation of nicotinic receptors likely has a prominent importance. The results of the present study support the hypothesis that harmane could be a tobacco (or smoke) component other than nicotine involved in tobacco dependence.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0014-2999</s0></fA01><fA02 i1="01"><s0>EJPHAZ</s0></fA02><fA03 i2="1"><s0>Eur. j. pharmacol.</s0></fA03><fA05><s2>629</s2></fA05><fA06><s2>1-3</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Electrophysiological characterization of harmane-induced activation of mesolimbic dopamine neurons</s1></fA08><fA11 i1="01" i2="1"><s1>ARIB (Ouafa)</s1></fA11><fA11 i1="02" i2="1"><s1>RAT (Pascal)</s1></fA11><fA11 i1="03" i2="1"><s1>MOLIMARD (Robert)</s1></fA11><fA11 i1="04" i2="1"><s1>CHAIT (Abderrahman)</s1></fA11><fA11 i1="05" i2="1"><s1>FAURE (Philippe)</s1></fA11><fA11 i1="06" i2="1"><s1>DE BEAUREPAIRE (Renaud)</s1></fA11><fA14 i1="01"><s1>Laboratoire de Psychopharmacologie, Centre Hospitalier Paul Guiraud, 54 avenue de la Republique</s1><s2>94806 Villejuif</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>6 aut.</sZ></fA14><fA14 i1="02"><s1>Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur</s1><s2>75724 Paris</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="03"><s1>Département de Biologie, Faculté Semlalia, Universit Cadi Ayyad</s1><s2>40 000 Marrakech</s2><s3>MAR</s3><sZ>4 aut.</sZ></fA14><fA20><s1>47-52</s1></fA20><fA21><s1>2010</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>13322</s2><s5>354000190111890080</s5></fA43><fA44><s0>0000</s0><s1>© 2010 INIST-CNRS. 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The effects of harmane were also tested after pre-treatment with the nicotine receptor antagonist mecamylamine. The results show that all substances, except befloxatone, activate the firing and/or burst activity of dopamine neurons. The increase in firing rate produced by harmane was approximately 18 times greater than that produced by nicotine. Such powerful excitation of dopamine neurons by harmane may in part explain its involvement in neurotoxicity, psychosis and addiction. The absence of effect of befloxatone supports the hypothesis that the effect of harmane is not related to its monoamine-oxidase-A inhibitory properties. Mecamylamine inhibited by approximately 80% the activity of harmane, indicating that the activating effect of harmane on dopamine neurons involves several mechanisms, among which activation of nicotinic receptors likely has a prominent importance. 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l="SPA"><s0>Antiparkinsoniano</s0><s5>26</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Psychotrope</s0><s2>FX</s2><s5>27</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Psychotropic</s0><s2>FX</s2><s5>27</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Psicotropo</s0><s2>FX</s2><s5>27</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Antidépresseur</s0><s5>28</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Antidepressant agent</s0><s5>28</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Antidepresor</s0><s5>28</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Harmane dérivé</s0><s4>INC</s4><s5>86</s5></fC03><fC03 i1="15" i2="X" l="FRE"><s0>β-Carboline dérivé</s0><s4>INC</s4><s5>87</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Oxidoreductases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Oxidoreductases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Oxidoreductases</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0><s2>FE</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Alcaloïde</s0><s5>37</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Alkaloid</s0><s5>37</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Alcaloide</s0><s5>37</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Inhibiteur de la monoamine oxidase B</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Monoamine oxidase B inhibitor</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Inhibidor monoamine oxidase B</s0><s5>38</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Inhibiteur enzyme</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Enzyme inhibitor</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Inhibidor enzima</s0><s5>39</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Inhibiteur de la monoamine oxidase A</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Monoamine oxidase A inhibitor</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Inhibidor monoamine oxidase A</s0><s5>40</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>41</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>41</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>41</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0><s5>42</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>42</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>42</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>43</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>43</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>43</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>44</s5></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>44</s5></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>44</s5></fC07><fC07 i1="11" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>45</s5></fC07><fC07 i1="11" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>45</s5></fC07><fC07 i1="11" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>45</s5></fC07><fN21><s1>095</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 10-0152691 INIST</NO><ET>Electrophysiological characterization of harmane-induced activation of mesolimbic dopamine neurons</ET><AU>ARIB (Ouafa); RAT (Pascal); MOLIMARD (Robert); CHAIT (Abderrahman); FAURE (Philippe); DE BEAUREPAIRE (Renaud)</AU><AF>Laboratoire de Psychopharmacologie, Centre Hospitalier Paul Guiraud, 54 avenue de la Republique/94806 Villejuif/France (1 aut., 2 aut., 3 aut., 6 aut.); Neurobiologie Intégrative des Systèmes Cholinergiques, Institut Pasteur/75724 Paris/France (1 aut., 5 aut.); Département de Biologie, Faculté Semlalia, Universit Cadi Ayyad/40 000 Marrakech/Maroc (4 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>European journal of pharmacology; ISSN 0014-2999; Coden EJPHAZ; Pays-Bas; Da. 2010; Vol. 629; No. 1-3; Pp. 47-52; Bibl. 1/4 p.</SO><LA>Anglais</LA><EA>It has been suggested that the beta-carbolines harmane and norharmane may be involved in the pathophysiology of Parkinson's disease, psychosis and addiction, but the mechanisms of these possible effects remain to be elucidated. In the present study, the effects of the two compounds were examined by using in vivo extracellular recordings of ventral tegmental dopamine neurons. The effects of harmane (2 mg/kg) and norharmane (2 mg/kg), were compared to those of nicotine (11 μg/kg), of cotinine (0.5 mg/kg), of the monoamine-oxidase-A inhibitor befloxatone (0.12 mg/kg), and of the monoamine-oxidase-B inhibitor selegiline (0.5 mg/kg). The effects of harmane were also tested after pre-treatment with the nicotine receptor antagonist mecamylamine. The results show that all substances, except befloxatone, activate the firing and/or burst activity of dopamine neurons. The increase in firing rate produced by harmane was approximately 18 times greater than that produced by nicotine. Such powerful excitation of dopamine neurons by harmane may in part explain its involvement in neurotoxicity, psychosis and addiction. The absence of effect of befloxatone supports the hypothesis that the effect of harmane is not related to its monoamine-oxidase-A inhibitory properties. Mecamylamine inhibited by approximately 80% the activity of harmane, indicating that the activating effect of harmane on dopamine neurons involves several mechanisms, among which activation of nicotinic receptors likely has a prominent importance. The results of the present study support the hypothesis that harmane could be a tobacco (or smoke) component other than nicotine involved in tobacco dependence.</EA><CC>002B02B06; 002B17G; 002B03E; 002B17A01</CC><FD>Electrophysiologie; Caractérisation; Neurone dopaminergique; Nicotine; Amine oxidase (flavin-containing); Sélégiline; Béfloxatone; Maladie de Parkinson; Psychose; Tabagisme; Antiparkinsonien; Psychotrope; Antidépresseur; Harmane dérivé; β-Carboline dérivé</FD><FG>Oxidoreductases; Enzyme; Alcaloïde; Inhibiteur de la monoamine oxidase B; Inhibiteur enzyme; Inhibiteur de la monoamine oxidase A; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central; Pathologie du système nerveux</FG><ED>Electrophysiology; Characterization; Dopaminergic neuron; Nicotine; Amine oxidase (flavin-containing); Selegiline; Befloxatone; Parkinson disease; Psychosis; Tobacco smoking; Antiparkinson agent; Psychotropic; Antidepressant agent</ED><EG>Oxidoreductases; Enzyme; Alkaloid; Monoamine oxidase B inhibitor; Enzyme inhibitor; Monoamine oxidase A inhibitor; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases</EG><SD>Electrofisiología; Caracterización; Neurona dopaminérgica; Nicotina; Amine oxidase (flavin-containing); Selegilina; Befloxatona; Parkinson enfermedad; Psicosis; Tabaquismo; Antiparkinsoniano; Psicotropo; Antidepresor</SD><LO>INIST-13322.354000190111890080</LO><ID>10-0152691</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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