Brain α7 nicotinic acetylcholine receptors in MPTP-lesioned monkeys and parkinsonian patients.
Identifieur interne : 000221 ( PubMed/Corpus ); précédent : 000220; suivant : 000222Brain α7 nicotinic acetylcholine receptors in MPTP-lesioned monkeys and parkinsonian patients.
Auteurs : Marc Morissette ; Nicolas Morin ; Laurent Grégoire ; Alex Rajput ; Ali H. Rajput ; Thérèse Di PaoloSource :
- 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
Links to Exploration step
pubmed:27038656Le document en format XML
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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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27038656</PMID><DateCreated><Year>2016</Year><Month>05</Month><Day>02</Day></DateCreated><DateCompleted><Year>2017</Year><Month>04</Month><Day>26</Day></DateCompleted><DateRevised><Year>2017</Year><Month>04</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-2968</ISSN><JournalIssue CitedMedium="Internet"><Volume>109</Volume><PubDate><Year>2016</Year><Month>Jun</Month><Day>01</Day></PubDate></JournalIssue><Title>Biochemical pharmacology</Title><ISOAbbreviation>Biochem. Pharmacol.</ISOAbbreviation></Journal><ArticleTitle>Brain α7 nicotinic acetylcholine receptors in MPTP-lesioned monkeys and parkinsonian patients.</ArticleTitle><Pagination><MedlinePgn>62-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.bcp.2016.03.023</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0006-2952(16)30004-1</ELocationID><Abstract><AbstractText>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.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Morissette</LastName><ForeName>Marc</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2, Canada. Electronic address: marc.morissette@crchudequebec.ulaval.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morin</LastName><ForeName>Nicolas</ForeName><Initials>N</Initials><AffiliationInfo><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.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Grégoire</LastName><ForeName>Laurent</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Neuroscience Research Unit, Centre de recherche du CHU de Québec, Quebec City G1V 4G2, Canada. Electronic address: laurent.gregoire@crchudequebec.ulaval.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rajput</LastName><ForeName>Alex</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Division of Neurology, University of Saskatchewan, Royal University Hospital, Saskatoon, SK S7N 0W8, Canada. Electronic address: ahr128@campus.usask.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rajput</LastName><ForeName>Ali H</ForeName><Initials>AH</Initials><AffiliationInfo><Affiliation>Division of Neurology, University of Saskatchewan, Royal University Hospital, Saskatoon, SK S7N 0W8, Canada. Electronic address: Ali.Rajput@saskatoonhealthregion.ca.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Di Paolo</LastName><ForeName>Thérèse</ForeName><Initials>T</Initials><AffiliationInfo><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.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>03</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Biochem Pharmacol</MedlineTA><NlmUniqueID>0101032</NlmUniqueID><ISSNLinking>0006-2952</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002038">Bungarotoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018691">Excitatory Amino Acid Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007457">Iodine Radioisotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011725">Pyridines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D064569">alpha7 Nicotinic Acetylcholine Receptor</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>7VC0YVI27Y</RegistryNumber><NameOfSubstance UI="C121465">6-methyl-2-(phenylethynyl)pyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="N">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000978" MajorTopicYN="N">Antiparkinson Agents</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002038" MajorTopicYN="N">Bungarotoxins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002421" MajorTopicYN="N">Caudate Nucleus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="N">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018691" MajorTopicYN="N">Excitatory Amino Acid Antagonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015870" MajorTopicYN="N">Gene Expression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007457" MajorTopicYN="N">Iodine Radioisotopes</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007980" MajorTopicYN="N">Levodopa</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008252" MajorTopicYN="N">Macaca fascicularis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009928" MajorTopicYN="N">Organ Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010052" MajorTopicYN="N">Ovariectomy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010300" MajorTopicYN="N">Parkinson Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011699" MajorTopicYN="N">Putamen</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011725" MajorTopicYN="N">Pyridines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D064569" MajorTopicYN="N">alpha7 Nicotinic Acetylcholine Receptor</DescriptorName><QualifierName UI="Q000819" MajorTopicYN="N">agonists</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Human</Keyword><Keyword MajorTopicYN="N">L-DOPA-induced dyskinesia</Keyword><Keyword MajorTopicYN="N">MPTP-lesioned monkey</Keyword><Keyword MajorTopicYN="N">Parkinson’s disease</Keyword><Keyword MajorTopicYN="N">α7 nicotinic acetylcholine receptor</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>02</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>03</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>4</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>4</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>4</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27038656</ArticleId><ArticleId IdType="pii">S0006-2952(16)30004-1</ArticleId><ArticleId IdType="doi">10.1016/j.bcp.2016.03.023</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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