Behavioral phenotyping of Parkin-deficient mice: looking for early preclinical features of Parkinson's disease.
Identifieur interne : 000450 ( PubMed/Corpus ); précédent : 000449; suivant : 000451Behavioral phenotyping of Parkin-deficient mice: looking for early preclinical features of Parkinson's disease.
Auteurs : Daniel Rial ; Adalberto A. Castro ; Nuno Machado ; Pedro Garção ; Francisco Q. Gonçalves ; Henrique B. Silva ; Angelo R. Tomé ; Attila Köfalvi ; Olga Corti ; Rita Raisman-Vozari ; Rodrigo A. Cunha ; Rui D. PredigerSource :
- PloS one [ 1932-6203 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Behavior, Animal, Disease Models, Animal, Dopamine (metabolism), Gene Deletion, Hippocampus (metabolism), Hippocampus (physiopathology), Homozygote, Locomotion, Long-Term Potentiation, Male, Memory, Mice, Mice, Knockout, Motor Activity, Nerve Endings (metabolism), Parkinson Disease (diagnosis), Parkinson Disease (genetics), Parkinson Disease (physiopathology), Phenotype, Ubiquitin-Protein Ligases (deficiency), Ubiquitin-Protein Ligases (genetics).
- MESH :
- chemical , deficiency : Ubiquitin-Protein Ligases.
- chemical , genetics : Ubiquitin-Protein Ligases.
- chemical , metabolism : Dopamine.
- diagnosis : Parkinson Disease.
- genetics : Parkinson Disease.
- metabolism : Hippocampus, Nerve Endings.
- physiopathology : Hippocampus, Parkinson Disease.
- Animals, Behavior, Animal, Disease Models, Animal, Gene Deletion, Homozygote, Locomotion, Long-Term Potentiation, Male, Memory, Mice, Mice, Knockout, Motor Activity, Phenotype.
Abstract
There is considerable evidence showing that the neurodegenerative processes that lead to sporadic Parkinson's disease (PD) begin many years before the appearance of the characteristic motor symptoms. Neuropsychiatric, sensorial and cognitive deficits are recognized as early non-motor manifestations of PD, and are not attenuated by the current anti-parkinsonian therapy. Although loss-of-function mutations in the parkin gene cause early-onset familial PD, Parkin-deficient mice do not display spontaneous degeneration of the nigrostriatal pathway or enhanced vulnerability to dopaminergic neurotoxins such as 6-OHDA and MPTP. Here, we employed adult homozygous C57BL/6 mice with parkin gene deletion on exon 3 (parkin-/-) to further investigate the relevance of Parkin in the regulation of non-motor features, namely olfactory, emotional, cognitive and hippocampal synaptic plasticity. Parkin-/- mice displayed normal performance on behavioral tests evaluating olfaction (olfactory discrimination), anxiety (elevated plus-maze), depressive-like behavior (forced swimming and tail suspension) and motor function (rotarod, grasping strength and pole). However, parkin-/- mice displayed a poor performance in the open field habituation, object location and modified Y-maze tasks suggestive of procedural and short-term spatial memory deficits. These behavioral impairments were accompanied by impaired hippocampal long-term potentiation (LTP). These findings indicate that the genetic deletion of parkin causes deficiencies in hippocampal synaptic plasticity, resulting in memory deficits with no major olfactory, emotional or motor impairments. Therefore, parkin-/- mice may represent a promising animal model to study the early stages of PD and for testing new therapeutic strategies to restore learning and memory and synaptic plasticity impairments in PD.
DOI: 10.1371/journal.pone.0114216
PubMed: 25486126
Links to Exploration step
pubmed:25486126Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Behavioral phenotyping of Parkin-deficient mice: looking for early preclinical features of Parkinson's disease.</title><author><name sortKey="Rial, Daniel" sort="Rial, Daniel" uniqKey="Rial D" first="Daniel" last="Rial">Daniel Rial</name><affiliation><nlm:affiliation>Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, UFSC, Florianópolis, 88049-900, SC, Brazil; CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Castro, Adalberto A" sort="Castro, Adalberto A" uniqKey="Castro A" first="Adalberto A" last="Castro">Adalberto A. Castro</name><affiliation><nlm:affiliation>Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, UFSC, Florianópolis, 88049-900, SC, Brazil.</nlm:affiliation></affiliation></author><author><name sortKey="Machado, Nuno" sort="Machado, Nuno" uniqKey="Machado N" first="Nuno" last="Machado">Nuno Machado</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Garcao, Pedro" sort="Garcao, Pedro" uniqKey="Garcao P" first="Pedro" last="Garção">Pedro Garção</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Goncalves, Francisco Q" sort="Goncalves, Francisco Q" uniqKey="Goncalves F" first="Francisco Q" last="Gonçalves">Francisco Q. 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Tomé</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal; Department of Life Sciences, Faculty of Sciences and Technology, University of Coimbra, 3000-456, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Kofalvi, Attila" sort="Kofalvi, Attila" uniqKey="Kofalvi A" first="Attila" last="Köfalvi">Attila Köfalvi</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Corti, Olga" sort="Corti, Olga" uniqKey="Corti O" first="Olga" last="Corti">Olga Corti</name><affiliation><nlm:affiliation>CNRS UMR 7225, Hôpital de la Salpêtrière-Bâtiment, ICM (Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière), CRICM, Thérapeutique Expérimentale de la Neurodégénérescence, Université Pierre et Marie Curie, UPMC, 75651, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Raisman Vozari, Rita" sort="Raisman Vozari, Rita" uniqKey="Raisman Vozari R" first="Rita" last="Raisman-Vozari">Rita Raisman-Vozari</name><affiliation><nlm:affiliation>CNRS UMR 7225, Hôpital de la Salpêtrière-Bâtiment, ICM (Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière), CRICM, Thérapeutique Expérimentale de la Neurodégénérescence, Université Pierre et Marie Curie, UPMC, 75651, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Cunha, Rodrigo A" sort="Cunha, Rodrigo A" uniqKey="Cunha R" first="Rodrigo A" last="Cunha">Rodrigo A. Cunha</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal; Faculty of Medicine, University of Coimbra, 3005-504, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Prediger, Rui D" sort="Prediger, Rui D" uniqKey="Prediger R" first="Rui D" last="Prediger">Rui D. Prediger</name><affiliation><nlm:affiliation>Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, UFSC, Florianópolis, 88049-900, SC, Brazil.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25486126</idno><idno type="pmid">25486126</idno><idno type="doi">10.1371/journal.pone.0114216</idno><idno type="wicri:Area/PubMed/Corpus">000450</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000450</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Behavioral phenotyping of Parkin-deficient mice: looking for early preclinical features of Parkinson's disease.</title><author><name sortKey="Rial, Daniel" sort="Rial, Daniel" uniqKey="Rial D" first="Daniel" last="Rial">Daniel Rial</name><affiliation><nlm:affiliation>Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, UFSC, Florianópolis, 88049-900, SC, Brazil; CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Castro, Adalberto A" sort="Castro, Adalberto A" uniqKey="Castro A" first="Adalberto A" last="Castro">Adalberto A. Castro</name><affiliation><nlm:affiliation>Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, UFSC, Florianópolis, 88049-900, SC, Brazil.</nlm:affiliation></affiliation></author><author><name sortKey="Machado, Nuno" sort="Machado, Nuno" uniqKey="Machado N" first="Nuno" last="Machado">Nuno Machado</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Garcao, Pedro" sort="Garcao, Pedro" uniqKey="Garcao P" first="Pedro" last="Garção">Pedro Garção</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Goncalves, Francisco Q" sort="Goncalves, Francisco Q" uniqKey="Goncalves F" first="Francisco Q" last="Gonçalves">Francisco Q. Gonçalves</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Silva, Henrique B" sort="Silva, Henrique B" uniqKey="Silva H" first="Henrique B" last="Silva">Henrique B. Silva</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Tome, Angelo R" sort="Tome, Angelo R" uniqKey="Tome A" first="Angelo R" last="Tomé">Angelo R. Tomé</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal; Department of Life Sciences, Faculty of Sciences and Technology, University of Coimbra, 3000-456, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Kofalvi, Attila" sort="Kofalvi, Attila" uniqKey="Kofalvi A" first="Attila" last="Köfalvi">Attila Köfalvi</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Corti, Olga" sort="Corti, Olga" uniqKey="Corti O" first="Olga" last="Corti">Olga Corti</name><affiliation><nlm:affiliation>CNRS UMR 7225, Hôpital de la Salpêtrière-Bâtiment, ICM (Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière), CRICM, Thérapeutique Expérimentale de la Neurodégénérescence, Université Pierre et Marie Curie, UPMC, 75651, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Raisman Vozari, Rita" sort="Raisman Vozari, Rita" uniqKey="Raisman Vozari R" first="Rita" last="Raisman-Vozari">Rita Raisman-Vozari</name><affiliation><nlm:affiliation>CNRS UMR 7225, Hôpital de la Salpêtrière-Bâtiment, ICM (Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière), CRICM, Thérapeutique Expérimentale de la Neurodégénérescence, Université Pierre et Marie Curie, UPMC, 75651, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Cunha, Rodrigo A" sort="Cunha, Rodrigo A" uniqKey="Cunha R" first="Rodrigo A" last="Cunha">Rodrigo A. Cunha</name><affiliation><nlm:affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal; Faculty of Medicine, University of Coimbra, 3005-504, Coimbra, Portugal.</nlm:affiliation></affiliation></author><author><name sortKey="Prediger, Rui D" sort="Prediger, Rui D" uniqKey="Prediger R" first="Rui D" last="Prediger">Rui D. Prediger</name><affiliation><nlm:affiliation>Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, UFSC, Florianópolis, 88049-900, SC, Brazil.</nlm:affiliation></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Behavior, Animal</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Gene Deletion</term><term>Hippocampus (metabolism)</term><term>Hippocampus (physiopathology)</term><term>Homozygote</term><term>Locomotion</term><term>Long-Term Potentiation</term><term>Male</term><term>Memory</term><term>Mice</term><term>Mice, Knockout</term><term>Motor Activity</term><term>Nerve Endings (metabolism)</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (physiopathology)</term><term>Phenotype</term><term>Ubiquitin-Protein Ligases (deficiency)</term><term>Ubiquitin-Protein Ligases (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hippocampus</term><term>Nerve Endings</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hippocampus</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Behavior, Animal</term><term>Disease Models, Animal</term><term>Gene Deletion</term><term>Homozygote</term><term>Locomotion</term><term>Long-Term Potentiation</term><term>Male</term><term>Memory</term><term>Mice</term><term>Mice, Knockout</term><term>Motor Activity</term><term>Phenotype</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is considerable evidence showing that the neurodegenerative processes that lead to sporadic Parkinson's disease (PD) begin many years before the appearance of the characteristic motor symptoms. Neuropsychiatric, sensorial and cognitive deficits are recognized as early non-motor manifestations of PD, and are not attenuated by the current anti-parkinsonian therapy. Although loss-of-function mutations in the parkin gene cause early-onset familial PD, Parkin-deficient mice do not display spontaneous degeneration of the nigrostriatal pathway or enhanced vulnerability to dopaminergic neurotoxins such as 6-OHDA and MPTP. Here, we employed adult homozygous C57BL/6 mice with parkin gene deletion on exon 3 (parkin-/-) to further investigate the relevance of Parkin in the regulation of non-motor features, namely olfactory, emotional, cognitive and hippocampal synaptic plasticity. Parkin-/- mice displayed normal performance on behavioral tests evaluating olfaction (olfactory discrimination), anxiety (elevated plus-maze), depressive-like behavior (forced swimming and tail suspension) and motor function (rotarod, grasping strength and pole). However, parkin-/- mice displayed a poor performance in the open field habituation, object location and modified Y-maze tasks suggestive of procedural and short-term spatial memory deficits. These behavioral impairments were accompanied by impaired hippocampal long-term potentiation (LTP). These findings indicate that the genetic deletion of parkin causes deficiencies in hippocampal synaptic plasticity, resulting in memory deficits with no major olfactory, emotional or motor impairments. Therefore, parkin-/- mice may represent a promising animal model to study the early stages of PD and for testing new therapeutic strategies to restore learning and memory and synaptic plasticity impairments in PD.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25486126</PMID><DateCreated><Year>2014</Year><Month>12</Month><Day>09</Day></DateCreated><DateCompleted><Year>2015</Year><Month>08</Month><Day>05</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>12</Issue><PubDate><Year>2014</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Behavioral phenotyping of Parkin-deficient mice: looking for early preclinical features of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>e114216</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0114216</ELocationID><Abstract><AbstractText>There is considerable evidence showing that the neurodegenerative processes that lead to sporadic Parkinson's disease (PD) begin many years before the appearance of the characteristic motor symptoms. Neuropsychiatric, sensorial and cognitive deficits are recognized as early non-motor manifestations of PD, and are not attenuated by the current anti-parkinsonian therapy. Although loss-of-function mutations in the parkin gene cause early-onset familial PD, Parkin-deficient mice do not display spontaneous degeneration of the nigrostriatal pathway or enhanced vulnerability to dopaminergic neurotoxins such as 6-OHDA and MPTP. Here, we employed adult homozygous C57BL/6 mice with parkin gene deletion on exon 3 (parkin-/-) to further investigate the relevance of Parkin in the regulation of non-motor features, namely olfactory, emotional, cognitive and hippocampal synaptic plasticity. Parkin-/- mice displayed normal performance on behavioral tests evaluating olfaction (olfactory discrimination), anxiety (elevated plus-maze), depressive-like behavior (forced swimming and tail suspension) and motor function (rotarod, grasping strength and pole). However, parkin-/- mice displayed a poor performance in the open field habituation, object location and modified Y-maze tasks suggestive of procedural and short-term spatial memory deficits. These behavioral impairments were accompanied by impaired hippocampal long-term potentiation (LTP). These findings indicate that the genetic deletion of parkin causes deficiencies in hippocampal synaptic plasticity, resulting in memory deficits with no major olfactory, emotional or motor impairments. Therefore, parkin-/- mice may represent a promising animal model to study the early stages of PD and for testing new therapeutic strategies to restore learning and memory and synaptic plasticity impairments in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rial</LastName><ForeName>Daniel</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, UFSC, Florianópolis, 88049-900, SC, Brazil; CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Castro</LastName><ForeName>Adalberto A</ForeName><Initials>AA</Initials><AffiliationInfo><Affiliation>Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, UFSC, Florianópolis, 88049-900, SC, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Machado</LastName><ForeName>Nuno</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Garção</LastName><ForeName>Pedro</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gonçalves</LastName><ForeName>Francisco Q</ForeName><Initials>FQ</Initials><AffiliationInfo><Affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Silva</LastName><ForeName>Henrique B</ForeName><Initials>HB</Initials><AffiliationInfo><Affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tomé</LastName><ForeName>Angelo R</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal; Department of Life Sciences, Faculty of Sciences and Technology, University of Coimbra, 3000-456, Coimbra, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Köfalvi</LastName><ForeName>Attila</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Corti</LastName><ForeName>Olga</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>CNRS UMR 7225, Hôpital de la Salpêtrière-Bâtiment, ICM (Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière), CRICM, Thérapeutique Expérimentale de la Neurodégénérescence, Université Pierre et Marie Curie, UPMC, 75651, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Raisman-Vozari</LastName><ForeName>Rita</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>CNRS UMR 7225, Hôpital de la Salpêtrière-Bâtiment, ICM (Centre de Recherche de l'Institut du Cerveau et de la Moelle épinière), CRICM, Thérapeutique Expérimentale de la Neurodégénérescence, Université Pierre et Marie Curie, UPMC, 75651, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cunha</LastName><ForeName>Rodrigo A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>CNC - Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal; Faculty of Medicine, University of Coimbra, 3005-504, Coimbra, Portugal.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Prediger</LastName><ForeName>Rui D</ForeName><Initials>RD</Initials><AffiliationInfo><Affiliation>Departamento de Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, UFSC, Florianópolis, 88049-900, SC, Brazil.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>12</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="C111567">parkin 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PubStatus="entrez"><Year>2014</Year><Month>12</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>12</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>8</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25486126</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0114216</ArticleId><ArticleId IdType="pii">PONE-D-14-39491</ArticleId><ArticleId IdType="pmc">PMC4259468</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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