Brain α7 nicotinic acetylcholine receptors in MPTP-lesioned monkeys and parkinsonian patients.
Identifieur interne : 000424 ( Main/Exploration ); précédent : 000423; suivant : 000425Brain α7 nicotinic acetylcholine receptors in MPTP-lesioned monkeys and parkinsonian patients.
Auteurs : Marc Morissette [Canada] ; Nicolas Morin [Canada] ; Laurent Grégoire [Canada] ; Alex Rajput [Canada] ; Ali H. Rajput [Canada] ; Thérèse Di Paolo [Canada]Source :
- Biochemical pharmacology [ 1873-2968 ] ; 2016.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (administration & dosage), Aged, Aged, 80 and over, Animals, Antiparkinson Agents (adverse effects), Bungarotoxins (metabolism), Case-Control Studies, Caudate Nucleus (drug effects), Caudate Nucleus (metabolism), Caudate Nucleus (pathology), Corpus Striatum (drug effects), Corpus Striatum (metabolism), Corpus Striatum (pathology), Dyskinesia, Drug-Induced (metabolism), Dyskinesia, Drug-Induced (physiopathology), Dyskinesia, Drug-Induced (prevention & control), Excitatory Amino Acid Antagonists (pharmacology), Female, Gene Expression, Humans, Iodine Radioisotopes, Levodopa (adverse effects), Macaca fascicularis, Male, Organ Specificity, Ovariectomy, Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (drug therapy), Parkinson Disease, Secondary (metabolism), Parkinson Disease, Secondary (pathology), Putamen (drug effects), Putamen (metabolism), Putamen (pathology), Pyridines (pharmacology), Signal Transduction, alpha7 Nicotinic Acetylcholine Receptor (agonists), alpha7 Nicotinic Acetylcholine Receptor (genetics), alpha7 Nicotinic Acetylcholine Receptor (metabolism).
- MESH :
- chemical , administration & dosage : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine.
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , agonists : alpha7 Nicotinic Acetylcholine Receptor.
- chemical , genetics : alpha7 Nicotinic Acetylcholine Receptor.
- chemical , metabolism : Bungarotoxins, alpha7 Nicotinic Acetylcholine Receptor.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Caudate Nucleus, Corpus Striatum, Putamen.
- drug therapy : Parkinson Disease, Parkinson Disease, Secondary.
- metabolism : Caudate Nucleus, Corpus Striatum, Dyskinesia, Drug-Induced, Parkinson Disease, Parkinson Disease, Secondary, Putamen.
- pathology : Caudate Nucleus, Corpus Striatum, Parkinson Disease, Parkinson Disease, Secondary, Putamen.
- chemical , pharmacology : Excitatory Amino Acid Antagonists, Pyridines.
- physiopathology : Dyskinesia, Drug-Induced.
- prevention & control : Dyskinesia, Drug-Induced.
- Aged, Aged, 80 and over, Animals, Case-Control Studies, Female, Gene Expression, Humans, Iodine Radioisotopes, Macaca fascicularis, Male, Organ Specificity, Ovariectomy, Signal Transduction.
Abstract
L-DOPA-induced dyskinesias (LID) appear in the majority of Parkinson's disease (PD) patients. Nicotinic acetylcholine (nACh) receptor-mediated signaling has been implicated in PD and LID and modulation of brain α7 nACh receptors might be a potential therapeutic target for PD. This study used [(125)I]α-Bungarotoxin autoradiography to investigate α7 nACh receptors in LID in post-mortem brains from PD patients (n=14) and control subjects (n=11), and from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys treated with saline (n=5), L-DOPA (n=4) or L-DOPA+2-methyl-6-(phenylethynyl)pyridine (MPEP) (n=5), and control monkeys (n=4). MPEP is the prototypal metabotropic glutamate 5 (mGlu5) receptor antagonist; it reduced the development of LID in these monkeys. [(125)I]α-Bungarotoxin specific binding to striatal and pallidal α7 nACh receptors were only increased in L-DOPA-treated dyskinetic MPTP monkeys as compared to controls, saline and L-DOPA+MPEP MPTP monkeys; dyskinesia scores correlated positively with this binding. The total group of Parkinsonian patients had higher [(125)I]α-Bungarotoxin specific binding compared to controls in the caudate nucleus but not in the putamen. PD patients without motor complications had higher [(125)I]α-Bungarotoxin specific binding compared to controls only in the caudate nucleus. PD patients with LID only had higher [(125)I]α-Bungarotoxin specific binding compared to controls in the caudate nucleus and compared to those without motor complications and controls in the putamen. PD patients with wearing-off only, had [(125)I]α-Bungarotoxin specific binding at control values in the caudate nucleus and lower in the putamen. Reduced motor complications were associated with normal striatal α7 nACh receptors, suggesting the potential of this receptor to manage motor complications in PD.
DOI: 10.1016/j.bcp.2016.03.023
PubMed: 27038656
Affiliations:
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Electronic address: laurent.gregoire@crchudequebec.ulaval.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2</wicri:regionArea><wicri:noRegion>Quebec City G1V 4G2</wicri:noRegion></affiliation></author><author><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><affiliation wicri:level="1"><nlm:affiliation>Division of Neurology, University of Saskatchewan, Royal University Hospital, Saskatoon, SK S7N 0W8, Canada. 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Electronic address: marc.morissette@crchudequebec.ulaval.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2</wicri:regionArea><wicri:noRegion>Quebec City G1V 4G2</wicri:noRegion></affiliation></author><author><name sortKey="Morin, Nicolas" sort="Morin, Nicolas" uniqKey="Morin N" first="Nicolas" last="Morin">Nicolas Morin</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Pharmacy, Université Laval, Quebec City G1K 7P4, Canada; Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2, Canada. Electronic address: nicolas.morin.4@ulaval.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Pharmacy, Université Laval, Quebec City G1K 7P4, Canada; Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2</wicri:regionArea><wicri:noRegion>Quebec City G1V 4G2</wicri:noRegion></affiliation></author><author><name sortKey="Gregoire, Laurent" sort="Gregoire, Laurent" uniqKey="Gregoire L" first="Laurent" last="Grégoire">Laurent Grégoire</name><affiliation wicri:level="1"><nlm:affiliation>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2, Canada. Electronic address: laurent.gregoire@crchudequebec.ulaval.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2</wicri:regionArea><wicri:noRegion>Quebec City G1V 4G2</wicri:noRegion></affiliation></author><author><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><affiliation wicri:level="1"><nlm:affiliation>Division of Neurology, University of Saskatchewan, Royal University Hospital, Saskatoon, SK S7N 0W8, Canada. 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Electronic address: Ali.Rajput@saskatoonhealthregion.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, University of Saskatchewan, Royal University Hospital, Saskatoon, SK S7N 0W8</wicri:regionArea><wicri:noRegion>SK S7N 0W8</wicri:noRegion></affiliation></author><author><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name><affiliation wicri:level="1"><nlm:affiliation>Faculty of Pharmacy, Université Laval, Quebec City G1K 7P4, Canada; Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2, Canada. Electronic address: therese.dipaolo@crchul.ulaval.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Faculty of Pharmacy, Université Laval, Quebec City G1K 7P4, Canada; Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2</wicri:regionArea><wicri:noRegion>Quebec City G1V 4G2</wicri:noRegion></affiliation></author></analytic><series><title level="j">Biochemical pharmacology</title><idno type="eISSN">1873-2968</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (administration & dosage)</term><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Antiparkinson Agents (adverse effects)</term><term>Bungarotoxins (metabolism)</term><term>Case-Control Studies</term><term>Caudate Nucleus (drug effects)</term><term>Caudate Nucleus (metabolism)</term><term>Caudate Nucleus (pathology)</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (metabolism)</term><term>Corpus Striatum (pathology)</term><term>Dyskinesia, Drug-Induced (metabolism)</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Dyskinesia, Drug-Induced (prevention & control)</term><term>Excitatory Amino Acid Antagonists (pharmacology)</term><term>Female</term><term>Gene Expression</term><term>Humans</term><term>Iodine Radioisotopes</term><term>Levodopa (adverse effects)</term><term>Macaca fascicularis</term><term>Male</term><term>Organ Specificity</term><term>Ovariectomy</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (drug therapy)</term><term>Parkinson Disease, Secondary (metabolism)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Putamen (drug effects)</term><term>Putamen (metabolism)</term><term>Putamen (pathology)</term><term>Pyridines (pharmacology)</term><term>Signal Transduction</term><term>alpha7 Nicotinic Acetylcholine Receptor (agonists)</term><term>alpha7 Nicotinic Acetylcholine Receptor (genetics)</term><term>alpha7 Nicotinic Acetylcholine Receptor (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>alpha7 Nicotinic Acetylcholine Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>alpha7 Nicotinic Acetylcholine Receptor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bungarotoxins</term><term>alpha7 Nicotinic Acetylcholine Receptor</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Caudate Nucleus</term><term>Corpus Striatum</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Caudate Nucleus</term><term>Corpus Striatum</term><term>Dyskinesia, Drug-Induced</term><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term><term>Putamen</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Caudate Nucleus</term><term>Corpus Striatum</term><term>Parkinson Disease</term><term>Parkinson Disease, Secondary</term><term>Putamen</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Excitatory Amino Acid Antagonists</term><term>Pyridines</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Animals</term><term>Case-Control Studies</term><term>Female</term><term>Gene Expression</term><term>Humans</term><term>Iodine Radioisotopes</term><term>Macaca fascicularis</term><term>Male</term><term>Organ Specificity</term><term>Ovariectomy</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">L-DOPA-induced dyskinesias (LID) appear in the majority of Parkinson's disease (PD) patients. Nicotinic acetylcholine (nACh) receptor-mediated signaling has been implicated in PD and LID and modulation of brain α7 nACh receptors might be a potential therapeutic target for PD. This study used [(125)I]α-Bungarotoxin autoradiography to investigate α7 nACh receptors in LID in post-mortem brains from PD patients (n=14) and control subjects (n=11), and from 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned monkeys treated with saline (n=5), L-DOPA (n=4) or L-DOPA+2-methyl-6-(phenylethynyl)pyridine (MPEP) (n=5), and control monkeys (n=4). MPEP is the prototypal metabotropic glutamate 5 (mGlu5) receptor antagonist; it reduced the development of LID in these monkeys. [(125)I]α-Bungarotoxin specific binding to striatal and pallidal α7 nACh receptors were only increased in L-DOPA-treated dyskinetic MPTP monkeys as compared to controls, saline and L-DOPA+MPEP MPTP monkeys; dyskinesia scores correlated positively with this binding. The total group of Parkinsonian patients had higher [(125)I]α-Bungarotoxin specific binding compared to controls in the caudate nucleus but not in the putamen. PD patients without motor complications had higher [(125)I]α-Bungarotoxin specific binding compared to controls only in the caudate nucleus. PD patients with LID only had higher [(125)I]α-Bungarotoxin specific binding compared to controls in the caudate nucleus and compared to those without motor complications and controls in the putamen. PD patients with wearing-off only, had [(125)I]α-Bungarotoxin specific binding at control values in the caudate nucleus and lower in the putamen. Reduced motor complications were associated with normal striatal α7 nACh receptors, suggesting the potential of this receptor to manage motor complications in PD.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Morissette, Marc" sort="Morissette, Marc" uniqKey="Morissette M" first="Marc" last="Morissette">Marc Morissette</name></noRegion><name sortKey="Di Paolo, Therese" sort="Di Paolo, Therese" uniqKey="Di Paolo T" first="Thérèse" last="Di Paolo">Thérèse Di Paolo</name><name sortKey="Gregoire, Laurent" sort="Gregoire, Laurent" uniqKey="Gregoire L" first="Laurent" last="Grégoire">Laurent Grégoire</name><name sortKey="Morin, Nicolas" sort="Morin, Nicolas" uniqKey="Morin N" first="Nicolas" last="Morin">Nicolas Morin</name><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><name sortKey="Rajput, Ali H" sort="Rajput, Ali H" uniqKey="Rajput A" first="Ali H" last="Rajput">Ali H. 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