Role of Nitric Oxide in Motor Control: Implications for Parkinson's Disease Pathophysiology and Treatment
Identifieur interne : 000368 ( PascalFrancis/Corpus ); précédent : 000367; suivant : 000369Role of Nitric Oxide in Motor Control: Implications for Parkinson's Disease Pathophysiology and Treatment
Auteurs : Elaine Del-Bel ; Fernando Eduardo Padovan-Neto ; Rita Raisman-Vozarl ; Marcio LazzariniSource :
- Current pharmaceutical design : (Print) [ 1381-6128 ] ; 2011.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
According to classical thinking about Parkinson's disease, loss of dopaminergic input from the substantia nigra pars compacta leads to overactivity and underactivity of the indirect and direct output pathways, respectively, in the basal ganglia. Administration of the dopamine precursor L-DOPA (1-3, 4-dihydroxyphenylalanine) is proposed to induce changes in the opposite directions. L-DOPA is the most used drug to treat Parkinson's disease symptoms. After repeated treatment with this compound, however, disabling secondary effects such as the abnormal involuntary movements usually appear. Nitric oxide is a free radical that can also acts as an atypical neurotransmitter and influences dopamine-mediated neurotransmission. In this paper we will briefly review the role of nitric oxide on motor control and in Parkinson's disease, particularly a possible role of nitric oxide in L-DOPA induced dyskinesia in rodents. Recent results show that nitric oxide synthase inhibition reduces L-DOPA-induced dyskinesia in rats and mice. The effect is dose-dependent, does not suffer tolerance nor interferes with L-DOPA positive motor effects. These preclinical findings suggest that nitric oxide is a promising therapeutic target for the reduction of L-DOPA-induced dyskinesia.
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Format Inist (serveur)
NO : | PASCAL 11-0416725 INIST |
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ET : | Role of Nitric Oxide in Motor Control: Implications for Parkinson's Disease Pathophysiology and Treatment |
AU : | DEL-BEL (Elaine); PADOVAN-NETO (Fernando Eduardo); RAISMAN-VOZARL (Rita); LAZZARINI (Marcio); HERRADON (Gonzalo) |
AF : | Medical School, Department of Behavioural Neuroscience, (FMRP-USP)/France (1 aut., 2 aut., 4 aut.); Dentistry School, Department of Physiology, (FORP-USP)/France (1 aut., 2 aut., 4 aut.); Inserm, UMR 975, CRICM, ICM, Thérapeutique Expérimental de la Neurodégénérescence/France (3 aut.); Université Pierre & Marie Curie-Paris, Faculté de Médecine/France (3 aut.); CNRS, UMR 7225/Paris, 75013/France (3 aut.); Department of Pharmaceutical and Food Sciences, Faculty of Pharmacy, University San Pablo CEU/Madrid/Espagne (1 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Current pharmaceutical design : (Print); ISSN 1381-6128; Emirats Arabes Unis; Da. 2011; Vol. 17; No. 5; Pp. 471-488; Bibl. 228 ref. |
LA : | Anglais |
EA : | According to classical thinking about Parkinson's disease, loss of dopaminergic input from the substantia nigra pars compacta leads to overactivity and underactivity of the indirect and direct output pathways, respectively, in the basal ganglia. Administration of the dopamine precursor L-DOPA (1-3, 4-dihydroxyphenylalanine) is proposed to induce changes in the opposite directions. L-DOPA is the most used drug to treat Parkinson's disease symptoms. After repeated treatment with this compound, however, disabling secondary effects such as the abnormal involuntary movements usually appear. Nitric oxide is a free radical that can also acts as an atypical neurotransmitter and influences dopamine-mediated neurotransmission. In this paper we will briefly review the role of nitric oxide on motor control and in Parkinson's disease, particularly a possible role of nitric oxide in L-DOPA induced dyskinesia in rodents. Recent results show that nitric oxide synthase inhibition reduces L-DOPA-induced dyskinesia in rats and mice. The effect is dose-dependent, does not suffer tolerance nor interferes with L-DOPA positive motor effects. These preclinical findings suggest that nitric oxide is a promising therapeutic target for the reduction of L-DOPA-induced dyskinesia. |
CC : | 002B17G; 002B17A01; 002B02B06 |
FD : | Monoxyde d'azote; Contrôle moteur; Maladie de Parkinson; Physiopathologie; Traitement; Inhibiteur de la NO synthase; Dopamine; Animal; Souris; Lévodopa; Dyskinésie; Mouvement anormal; Mouvement involontaire; Article synthèse |
FG : | Rodentia; Mammalia; Vertebrata; Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Catécholamine; Neurotransmetteur; Agoniste; Récepteur dopaminergique D2; Antiparkinsonien; Trouble neurologique |
ED : | Nitric oxide; Motor control; Parkinson disease; Pathophysiology; Treatment; Nitric oxide synthase inhibitor; Dopamine; Animal; Mouse; Levodopa; Dyskinesia; Abnormal movement; Involuntary movement; Review |
EG : | Rodentia; Mammalia; Vertebrata; Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Catecholamine; Neurotransmitter; Agonist; D2 Dopamine receptor; Antiparkinson agent; Neurological disorder |
SD : | Nitrógeno monóxido; Control motor; Parkinson enfermedad; Fisiopatología; Tratamiento; Inhibidor NO synthase; Dopamina; Animal; Ratón; Levodopa; Disquinesia; Movimiento anormal; Movimiento involuntario; Artículo síntesis |
LO : | INIST-26320.354000189800790060 |
ID : | 11-0416725 |
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Pascal:11-0416725Le document en format XML
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<front><div type="abstract" xml:lang="en">According to classical thinking about Parkinson's disease, loss of dopaminergic input from the substantia nigra pars compacta leads to overactivity and underactivity of the indirect and direct output pathways, respectively, in the basal ganglia. Administration of the dopamine precursor L-DOPA (1-3, 4-dihydroxyphenylalanine) is proposed to induce changes in the opposite directions. L-DOPA is the most used drug to treat Parkinson's disease symptoms. After repeated treatment with this compound, however, disabling secondary effects such as the abnormal involuntary movements usually appear. Nitric oxide is a free radical that can also acts as an atypical neurotransmitter and influences dopamine-mediated neurotransmission. In this paper we will briefly review the role of nitric oxide on motor control and in Parkinson's disease, particularly a possible role of nitric oxide in L-DOPA induced dyskinesia in rodents. Recent results show that nitric oxide synthase inhibition reduces L-DOPA-induced dyskinesia in rats and mice. The effect is dose-dependent, does not suffer tolerance nor interferes with L-DOPA positive motor effects. These preclinical findings suggest that nitric oxide is a promising therapeutic target for the reduction of L-DOPA-induced dyskinesia.</div>
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<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Dyskinésie</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Dyskinesia</s0>
<s5>12</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Disquinesia</s0>
<s5>12</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE"><s0>Mouvement anormal</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG"><s0>Abnormal movement</s0>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA"><s0>Movimiento anormal</s0>
<s5>13</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE"><s0>Mouvement involontaire</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG"><s0>Involuntary movement</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA"><s0>Movimiento involuntario</s0>
<s5>14</s5>
</fC03>
<fC03 i1="14" i2="X" l="FRE"><s0>Article synthèse</s0>
<s5>15</s5>
</fC03>
<fC03 i1="14" i2="X" l="ENG"><s0>Review</s0>
<s5>15</s5>
</fC03>
<fC03 i1="14" i2="X" l="SPA"><s0>Artículo síntesis</s0>
<s5>15</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>37</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>37</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>38</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>39</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Catécholamine</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Catecholamine</s0>
<s5>42</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Catecolamina</s0>
<s5>42</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Neurotransmetteur</s0>
<s5>43</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Neurotransmitter</s0>
<s5>43</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Neurotransmisor</s0>
<s5>43</s5>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Agoniste</s0>
<s5>44</s5>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Agonist</s0>
<s5>44</s5>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Agonista</s0>
<s5>44</s5>
</fC07>
<fC07 i1="12" i2="X" l="FRE"><s0>Récepteur dopaminergique D2</s0>
<s5>45</s5>
</fC07>
<fC07 i1="12" i2="X" l="ENG"><s0>D2 Dopamine receptor</s0>
<s5>45</s5>
</fC07>
<fC07 i1="12" i2="X" l="SPA"><s0>Receptor dopaminérgico D2</s0>
<s5>45</s5>
</fC07>
<fC07 i1="13" i2="X" l="FRE"><s0>Antiparkinsonien</s0>
<s5>46</s5>
</fC07>
<fC07 i1="13" i2="X" l="ENG"><s0>Antiparkinson agent</s0>
<s5>46</s5>
</fC07>
<fC07 i1="13" i2="X" l="SPA"><s0>Antiparkinsoniano</s0>
<s5>46</s5>
</fC07>
<fC07 i1="14" i2="X" l="FRE"><s0>Trouble neurologique</s0>
<s5>47</s5>
</fC07>
<fC07 i1="14" i2="X" l="ENG"><s0>Neurological disorder</s0>
<s5>47</s5>
</fC07>
<fC07 i1="14" i2="X" l="SPA"><s0>Trastorno neurológico</s0>
<s5>47</s5>
</fC07>
<fN21><s1>283</s1>
</fN21>
</pA>
</standard>
<server><NO>PASCAL 11-0416725 INIST</NO>
<ET>Role of Nitric Oxide in Motor Control: Implications for Parkinson's Disease Pathophysiology and Treatment</ET>
<AU>DEL-BEL (Elaine); PADOVAN-NETO (Fernando Eduardo); RAISMAN-VOZARL (Rita); LAZZARINI (Marcio); HERRADON (Gonzalo)</AU>
<AF>Medical School, Department of Behavioural Neuroscience, (FMRP-USP)/France (1 aut., 2 aut., 4 aut.); Dentistry School, Department of Physiology, (FORP-USP)/France (1 aut., 2 aut., 4 aut.); Inserm, UMR 975, CRICM, ICM, Thérapeutique Expérimental de la Neurodégénérescence/France (3 aut.); Université Pierre & Marie Curie-Paris, Faculté de Médecine/France (3 aut.); CNRS, UMR 7225/Paris, 75013/France (3 aut.); Department of Pharmaceutical and Food Sciences, Faculty of Pharmacy, University San Pablo CEU/Madrid/Espagne (1 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Current pharmaceutical design : (Print); ISSN 1381-6128; Emirats Arabes Unis; Da. 2011; Vol. 17; No. 5; Pp. 471-488; Bibl. 228 ref.</SO>
<LA>Anglais</LA>
<EA>According to classical thinking about Parkinson's disease, loss of dopaminergic input from the substantia nigra pars compacta leads to overactivity and underactivity of the indirect and direct output pathways, respectively, in the basal ganglia. Administration of the dopamine precursor L-DOPA (1-3, 4-dihydroxyphenylalanine) is proposed to induce changes in the opposite directions. L-DOPA is the most used drug to treat Parkinson's disease symptoms. After repeated treatment with this compound, however, disabling secondary effects such as the abnormal involuntary movements usually appear. Nitric oxide is a free radical that can also acts as an atypical neurotransmitter and influences dopamine-mediated neurotransmission. In this paper we will briefly review the role of nitric oxide on motor control and in Parkinson's disease, particularly a possible role of nitric oxide in L-DOPA induced dyskinesia in rodents. Recent results show that nitric oxide synthase inhibition reduces L-DOPA-induced dyskinesia in rats and mice. The effect is dose-dependent, does not suffer tolerance nor interferes with L-DOPA positive motor effects. These preclinical findings suggest that nitric oxide is a promising therapeutic target for the reduction of L-DOPA-induced dyskinesia.</EA>
<CC>002B17G; 002B17A01; 002B02B06</CC>
<FD>Monoxyde d'azote; Contrôle moteur; Maladie de Parkinson; Physiopathologie; Traitement; Inhibiteur de la NO synthase; Dopamine; Animal; Souris; Lévodopa; Dyskinésie; Mouvement anormal; Mouvement involontaire; Article synthèse</FD>
<FG>Rodentia; Mammalia; Vertebrata; Maladie dégénérative; Pathologie du système nerveux; Pathologie de l'encéphale; Syndrome extrapyramidal; Pathologie du système nerveux central; Catécholamine; Neurotransmetteur; Agoniste; Récepteur dopaminergique D2; Antiparkinsonien; Trouble neurologique</FG>
<ED>Nitric oxide; Motor control; Parkinson disease; Pathophysiology; Treatment; Nitric oxide synthase inhibitor; Dopamine; Animal; Mouse; Levodopa; Dyskinesia; Abnormal movement; Involuntary movement; Review</ED>
<EG>Rodentia; Mammalia; Vertebrata; Degenerative disease; Nervous system diseases; Cerebral disorder; Extrapyramidal syndrome; Central nervous system disease; Catecholamine; Neurotransmitter; Agonist; D2 Dopamine receptor; Antiparkinson agent; Neurological disorder</EG>
<SD>Nitrógeno monóxido; Control motor; Parkinson enfermedad; Fisiopatología; Tratamiento; Inhibidor NO synthase; Dopamina; Animal; Ratón; Levodopa; Disquinesia; Movimiento anormal; Movimiento involuntario; Artículo síntesis</SD>
<LO>INIST-26320.354000189800790060</LO>
<ID>11-0416725</ID>
</server>
</inist>
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