Basal ganglia serotonin 1B receptors in parkinsonian monkeys with L-DOPA-induced dyskinesia.
Identifieur interne : 000853 ( PubMed/Curation ); précédent : 000852; suivant : 000854Basal ganglia serotonin 1B receptors in parkinsonian monkeys with L-DOPA-induced dyskinesia.
Auteurs : Golnasim Riahi ; Marc Morissette ; Pershia Samadi ; Martin Parent ; Thérèse Di PaoloSource :
- Biochemical pharmacology [ 1873-2968 ] ; 2013.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (pharmacology), Animals, Autoradiography, Basal Ganglia (drug effects), Basal Ganglia (metabolism), Behavior, Animal (drug effects), Benzamides (metabolism), Brain (drug effects), Brain (metabolism), Case-Control Studies, Dyskinesia, Drug-Induced (metabolism), Dyskinesia, Drug-Induced (prevention & control), Levodopa (adverse effects), Macaca fascicularis, Parkinson Disease (metabolism), Pyridines (metabolism), Receptor, Serotonin, 5-HT1B (metabolism), Serotonin (metabolism), Sulfonamides (pharmacology), Thiazoles (pharmacology).
- MESH :
- chemical , adverse effects : Levodopa.
- chemical , metabolism : Benzamides, Pyridines, Receptor, Serotonin, 5-HT1B, Serotonin.
- chemical , pharmacology : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Sulfonamides, Thiazoles.
- drug effects : Basal Ganglia, Behavior, Animal, Brain.
- metabolism : Basal Ganglia, Brain, Dyskinesia, Drug-Induced, Parkinson Disease.
- prevention & control : Dyskinesia, Drug-Induced.
- Animals, Autoradiography, Case-Control Studies, Macaca fascicularis.
Abstract
L-DOPA-induced dyskinesias (LID)s are abnormal involuntary movements limiting the chronic use of L-DOPA, the main pharmacological treatment of Parkinson's disease (PD). Serotonin receptors are thought to contribute to LID but serotonin 1B (5-HT1B) receptors have never been investigated in any primate models of PD and LID. Therefore, we measured 5-HT1B receptors with [(3)H]GR 125743 autoradiography in controls, MPTP-lesioned monkeys, and L-DOPA-treated MPTP monkeys, with or without Ro 61-8048 treatment, a kynurenine hydroxylase inhibitor alleviating LID. In normal condition, 5-HT1B receptor specific binding was highest in the substantia nigra pars reticulata (SNr), high in the globus pallidus (GP), nucleus accumbens and substantia innominata and lower in the caudate nucleus and putamen. 5-HT1B receptors were increased in caudate nucleus, putamen and SNr of MPTP monkeys compared to controls. L-DOPA-treated MPTP monkeys had elevated 5-HT1B receptor specific binding in caudate nucleus, putamen, SNr and internal GP. In all these brain regions, increases were prevented by co-administration of Ro 61-8048. No effect of MPTP lesion or treatment was observed for 5-HT1B specific binding in the external GP, nucleus accumbens and substantia innominata. This study is the first description in primates of altered brain 5-HT1B receptors associated with prevention of LID.
DOI: 10.1016/j.bcp.2013.08.005
PubMed: 23954709
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Golnasim Riahi<affiliation><nlm:affiliation>Faculty of Pharmacy, Université Laval, Quebec City, Canada, G1K 7P4; Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City, Canada, G1V 4G2; Centre de Recherche de l'Institut universitaire en santé mentale de Québec, Quebec City, Canada, G1J 2G3.</nlm:affiliation>
<wicri:noCountry code="subField">G1J 2G3</wicri:noCountry>
</affiliation>
Le document en format XML
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<front><div type="abstract" xml:lang="en">L-DOPA-induced dyskinesias (LID)s are abnormal involuntary movements limiting the chronic use of L-DOPA, the main pharmacological treatment of Parkinson's disease (PD). Serotonin receptors are thought to contribute to LID but serotonin 1B (5-HT1B) receptors have never been investigated in any primate models of PD and LID. Therefore, we measured 5-HT1B receptors with [(3)H]GR 125743 autoradiography in controls, MPTP-lesioned monkeys, and L-DOPA-treated MPTP monkeys, with or without Ro 61-8048 treatment, a kynurenine hydroxylase inhibitor alleviating LID. In normal condition, 5-HT1B receptor specific binding was highest in the substantia nigra pars reticulata (SNr), high in the globus pallidus (GP), nucleus accumbens and substantia innominata and lower in the caudate nucleus and putamen. 5-HT1B receptors were increased in caudate nucleus, putamen and SNr of MPTP monkeys compared to controls. L-DOPA-treated MPTP monkeys had elevated 5-HT1B receptor specific binding in caudate nucleus, putamen, SNr and internal GP. In all these brain regions, increases were prevented by co-administration of Ro 61-8048. No effect of MPTP lesion or treatment was observed for 5-HT1B specific binding in the external GP, nucleus accumbens and substantia innominata. This study is the first description in primates of altered brain 5-HT1B receptors associated with prevention of LID.</div>
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<Abstract><AbstractText>L-DOPA-induced dyskinesias (LID)s are abnormal involuntary movements limiting the chronic use of L-DOPA, the main pharmacological treatment of Parkinson's disease (PD). Serotonin receptors are thought to contribute to LID but serotonin 1B (5-HT1B) receptors have never been investigated in any primate models of PD and LID. Therefore, we measured 5-HT1B receptors with [(3)H]GR 125743 autoradiography in controls, MPTP-lesioned monkeys, and L-DOPA-treated MPTP monkeys, with or without Ro 61-8048 treatment, a kynurenine hydroxylase inhibitor alleviating LID. In normal condition, 5-HT1B receptor specific binding was highest in the substantia nigra pars reticulata (SNr), high in the globus pallidus (GP), nucleus accumbens and substantia innominata and lower in the caudate nucleus and putamen. 5-HT1B receptors were increased in caudate nucleus, putamen and SNr of MPTP monkeys compared to controls. L-DOPA-treated MPTP monkeys had elevated 5-HT1B receptor specific binding in caudate nucleus, putamen, SNr and internal GP. In all these brain regions, increases were prevented by co-administration of Ro 61-8048. No effect of MPTP lesion or treatment was observed for 5-HT1B specific binding in the external GP, nucleus accumbens and substantia innominata. This study is the first description in primates of altered brain 5-HT1B receptors associated with prevention of LID.</AbstractText>
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