Compensatory T-type Ca2+ channel activity alters D2-autoreceptor responses of Substantia nigra dopamine neurons from Cav1.3 L-type Ca2+ channel KO mice.
Identifieur interne : 000559 ( PubMed/Checkpoint ); précédent : 000558; suivant : 000560Compensatory T-type Ca2+ channel activity alters D2-autoreceptor responses of Substantia nigra dopamine neurons from Cav1.3 L-type Ca2+ channel KO mice.
Auteurs : Christina Poetschke [Allemagne] ; Elena Dragicevic [Allemagne] ; Johanna Duda [Allemagne] ; Julia Benkert [Allemagne] ; Antonios Dougalis [Allemagne] ; Roberta Dezio [Allemagne] ; Terrance P. Snutch [Canada] ; Joerg Striessnig [Autriche] ; Birgit Liss [Allemagne]Source :
- Scientific reports [ 2045-2322 ] ; 2015.
English descriptors
- KwdEn :
- Age Factors, Animals, Autoreceptors (metabolism), Calcium (metabolism), Calcium Channel Blockers (pharmacology), Calcium Channels, L-Type (deficiency), Calcium Channels, T-Type (genetics), Calcium Channels, T-Type (metabolism), Dopaminergic Neurons (drug effects), Dopaminergic Neurons (metabolism), Gene Expression Regulation, Male, Membrane Potentials, Mice, Mice, Knockout, Neuronal Calcium-Sensor Proteins (genetics), Neuronal Calcium-Sensor Proteins (metabolism), Neuropeptides (genetics), Neuropeptides (metabolism), Parkinson Disease (genetics), Parkinson Disease (metabolism), Phenotype, RNA, Messenger (genetics), RNA, Messenger (metabolism), Receptors, Dopamine D2 (metabolism), Substantia Nigra (metabolism).
- MESH :
- chemical , deficiency : Calcium Channels, L-Type.
- chemical , genetics : Calcium Channels, T-Type, Neuronal Calcium-Sensor Proteins, Neuropeptides, RNA, Messenger.
- chemical , metabolism : Autoreceptors, Calcium, Calcium Channels, T-Type, Neuronal Calcium-Sensor Proteins, Neuropeptides, RNA, Messenger, Receptors, Dopamine D2.
- chemical , pharmacology : Calcium Channel Blockers.
- drug effects : Dopaminergic Neurons.
- genetics : Parkinson Disease.
- metabolism : Dopaminergic Neurons, Parkinson Disease, Substantia Nigra.
- Age Factors, Animals, Gene Expression Regulation, Male, Membrane Potentials, Mice, Mice, Knockout, Phenotype.
Abstract
The preferential degeneration of Substantia nigra dopamine midbrain neurons (SN DA) causes the motor-symptoms of Parkinson's disease (PD). Voltage-gated L-type calcium channels (LTCCs), especially the Cav1.3-subtype, generate an activity-related oscillatory Ca(2+) burden in SN DA neurons, contributing to their degeneration and PD. While LTCC-blockers are already in clinical trials as PD-therapy, age-dependent functional roles of Cav1.3 LTCCs in SN DA neurons remain unclear. Thus, we analysed juvenile and adult Cav1.3-deficient mice with electrophysiological and molecular techniques. To unmask compensatory effects, we compared Cav1.3 KO mice with pharmacological LTCC-inhibition. LTCC-function was not necessary for SN DA pacemaker-activity at either age, but rather contributed to their pacemaker-precision. Moreover, juvenile Cav1.3 KO but not WT mice displayed adult wildtype-like, sensitised inhibitory dopamine-D2-autoreceptor (D2-AR) responses that depended upon both, interaction of the neuronal calcium sensor NCS-1 with D2-ARs, and on voltage-gated T-type calcium channel (TTCC) activity. This functional KO-phenotype was accompanied by cell-specific up-regulation of NCS-1 and Cav3.1-TTCC mRNA. Furthermore, in wildtype we identified an age-dependent switch of TTCC-function from contributing to SN DA pacemaker-precision in juveniles to pacemaker-frequency in adults. This novel interplay of Cav1.3 L-type and Cav3.1 T-type channels, and their modulation of SN DA activity-pattern and D2-AR-sensitisation, provide new insights into flexible age- and calcium-dependent activity-control of SN DA neurons and its pharmacological modulation.
DOI: 10.1038/srep13688
PubMed: 26381090
Affiliations:
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Snutch</name><affiliation wicri:level="1"><nlm:affiliation>Djavad Mowafaghian Centre for Brain and Health and Michael Smith Laboratories, University of British Columbia, V6T1Z4 Vancouver, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Djavad Mowafaghian Centre for Brain and Health and Michael Smith Laboratories, University of British Columbia, V6T1Z4 Vancouver</wicri:regionArea><wicri:noRegion>V6T1Z4 Vancouver</wicri:noRegion></affiliation></author><author><name sortKey="Striessnig, Joerg" sort="Striessnig, Joerg" uniqKey="Striessnig J" first="Joerg" last="Striessnig">Joerg Striessnig</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Department of Pharmacology and Toxicology, University of Innsbruck, 6020 Innsbruck, Austria.</nlm:affiliation><country xml:lang="fr">Autriche</country><wicri:regionArea>Institute of Pharmacy, Department of Pharmacology and Toxicology, University of Innsbruck, 6020 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Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Applied Physiology, University of Ulm, 89081 Ulm</wicri:regionArea><wicri:noRegion>89081 Ulm</wicri:noRegion><orgName type="university">Université d'Ulm</orgName><placeName><settlement type="city">Ulm</settlement><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Tübingen</region></placeName></affiliation></author><author><name sortKey="Dragicevic, Elena" sort="Dragicevic, Elena" uniqKey="Dragicevic E" first="Elena" last="Dragicevic">Elena Dragicevic</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Applied Physiology, University of Ulm, 89081 Ulm</wicri:regionArea><wicri:noRegion>89081 Ulm</wicri:noRegion><orgName type="university">Université d'Ulm</orgName><placeName><settlement type="city">Ulm</settlement><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Tübingen</region></placeName></affiliation></author><author><name sortKey="Duda, Johanna" sort="Duda, Johanna" uniqKey="Duda J" first="Johanna" last="Duda">Johanna Duda</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Applied Physiology, University of Ulm, 89081 Ulm</wicri:regionArea><wicri:noRegion>89081 Ulm</wicri:noRegion><orgName type="university">Université d'Ulm</orgName><placeName><settlement type="city">Ulm</settlement><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Tübingen</region></placeName></affiliation></author><author><name sortKey="Benkert, Julia" sort="Benkert, Julia" uniqKey="Benkert J" first="Julia" last="Benkert">Julia Benkert</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Applied Physiology, University of Ulm, 89081 Ulm</wicri:regionArea><wicri:noRegion>89081 Ulm</wicri:noRegion><orgName type="university">Université d'Ulm</orgName><placeName><settlement type="city">Ulm</settlement><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Tübingen</region></placeName></affiliation></author><author><name sortKey="Dougalis, Antonios" sort="Dougalis, Antonios" uniqKey="Dougalis A" first="Antonios" last="Dougalis">Antonios Dougalis</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Applied Physiology, University of Ulm, 89081 Ulm</wicri:regionArea><wicri:noRegion>89081 Ulm</wicri:noRegion><orgName type="university">Université d'Ulm</orgName><placeName><settlement type="city">Ulm</settlement><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Tübingen</region></placeName></affiliation></author><author><name sortKey="Dezio, Roberta" sort="Dezio, Roberta" uniqKey="Dezio R" first="Roberta" last="Dezio">Roberta Dezio</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Applied Physiology, University of Ulm, 89081 Ulm</wicri:regionArea><wicri:noRegion>89081 Ulm</wicri:noRegion><orgName type="university">Université d'Ulm</orgName><placeName><settlement type="city">Ulm</settlement><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Tübingen</region></placeName></affiliation></author><author><name sortKey="Snutch, Terrance P" sort="Snutch, Terrance P" uniqKey="Snutch T" first="Terrance P" last="Snutch">Terrance P. Snutch</name><affiliation wicri:level="1"><nlm:affiliation>Djavad Mowafaghian Centre for Brain and Health and Michael Smith Laboratories, University of British Columbia, V6T1Z4 Vancouver, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Djavad Mowafaghian Centre for Brain and Health and Michael Smith Laboratories, University of British Columbia, V6T1Z4 Vancouver</wicri:regionArea><wicri:noRegion>V6T1Z4 Vancouver</wicri:noRegion></affiliation></author><author><name sortKey="Striessnig, Joerg" sort="Striessnig, Joerg" uniqKey="Striessnig J" first="Joerg" last="Striessnig">Joerg Striessnig</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmacy, Department of Pharmacology and Toxicology, University of Innsbruck, 6020 Innsbruck, Austria.</nlm:affiliation><country xml:lang="fr">Autriche</country><wicri:regionArea>Institute of Pharmacy, Department of Pharmacology and Toxicology, University of Innsbruck, 6020 Innsbruck</wicri:regionArea><wicri:noRegion>6020 Innsbruck</wicri:noRegion></affiliation></author><author><name sortKey="Liss, Birgit" sort="Liss, Birgit" uniqKey="Liss B" first="Birgit" last="Liss">Birgit Liss</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Applied Physiology, University of Ulm, 89081 Ulm</wicri:regionArea><wicri:noRegion>89081 Ulm</wicri:noRegion><orgName type="university">Université d'Ulm</orgName><placeName><settlement type="city">Ulm</settlement><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Tübingen</region></placeName></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Age Factors</term><term>Animals</term><term>Autoreceptors (metabolism)</term><term>Calcium (metabolism)</term><term>Calcium Channel Blockers (pharmacology)</term><term>Calcium Channels, L-Type (deficiency)</term><term>Calcium Channels, T-Type (genetics)</term><term>Calcium Channels, T-Type (metabolism)</term><term>Dopaminergic Neurons (drug effects)</term><term>Dopaminergic Neurons (metabolism)</term><term>Gene Expression Regulation</term><term>Male</term><term>Membrane Potentials</term><term>Mice</term><term>Mice, Knockout</term><term>Neuronal Calcium-Sensor Proteins (genetics)</term><term>Neuronal Calcium-Sensor Proteins (metabolism)</term><term>Neuropeptides (genetics)</term><term>Neuropeptides (metabolism)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Phenotype</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Receptors, Dopamine D2 (metabolism)</term><term>Substantia Nigra (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Calcium Channels, L-Type</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Calcium Channels, T-Type</term><term>Neuronal Calcium-Sensor Proteins</term><term>Neuropeptides</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Autoreceptors</term><term>Calcium</term><term>Calcium Channels, T-Type</term><term>Neuronal Calcium-Sensor Proteins</term><term>Neuropeptides</term><term>RNA, Messenger</term><term>Receptors, Dopamine D2</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Calcium Channel Blockers</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Dopaminergic Neurons</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dopaminergic Neurons</term><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Age Factors</term><term>Animals</term><term>Gene Expression Regulation</term><term>Male</term><term>Membrane Potentials</term><term>Mice</term><term>Mice, Knockout</term><term>Phenotype</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The preferential degeneration of Substantia nigra dopamine midbrain neurons (SN DA) causes the motor-symptoms of Parkinson's disease (PD). Voltage-gated L-type calcium channels (LTCCs), especially the Cav1.3-subtype, generate an activity-related oscillatory Ca(2+) burden in SN DA neurons, contributing to their degeneration and PD. While LTCC-blockers are already in clinical trials as PD-therapy, age-dependent functional roles of Cav1.3 LTCCs in SN DA neurons remain unclear. Thus, we analysed juvenile and adult Cav1.3-deficient mice with electrophysiological and molecular techniques. To unmask compensatory effects, we compared Cav1.3 KO mice with pharmacological LTCC-inhibition. LTCC-function was not necessary for SN DA pacemaker-activity at either age, but rather contributed to their pacemaker-precision. Moreover, juvenile Cav1.3 KO but not WT mice displayed adult wildtype-like, sensitised inhibitory dopamine-D2-autoreceptor (D2-AR) responses that depended upon both, interaction of the neuronal calcium sensor NCS-1 with D2-ARs, and on voltage-gated T-type calcium channel (TTCC) activity. This functional KO-phenotype was accompanied by cell-specific up-regulation of NCS-1 and Cav3.1-TTCC mRNA. Furthermore, in wildtype we identified an age-dependent switch of TTCC-function from contributing to SN DA pacemaker-precision in juveniles to pacemaker-frequency in adults. This novel interplay of Cav1.3 L-type and Cav3.1 T-type channels, and their modulation of SN DA activity-pattern and D2-AR-sensitisation, provide new insights into flexible age- and calcium-dependent activity-control of SN DA neurons and its pharmacological modulation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26381090</PMID><DateCreated><Year>2015</Year><Month>09</Month><Day>19</Day></DateCreated><DateCompleted><Year>2016</Year><Month>08</Month><Day>19</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>5</Volume><PubDate><Year>2015</Year><Month>Sep</Month><Day>18</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Compensatory T-type Ca2+ channel activity alters D2-autoreceptor responses of Substantia nigra dopamine neurons from Cav1.3 L-type Ca2+ channel KO mice.</ArticleTitle><Pagination><MedlinePgn>13688</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/srep13688</ELocationID><Abstract><AbstractText>The preferential degeneration of Substantia nigra dopamine midbrain neurons (SN DA) causes the motor-symptoms of Parkinson's disease (PD). Voltage-gated L-type calcium channels (LTCCs), especially the Cav1.3-subtype, generate an activity-related oscillatory Ca(2+) burden in SN DA neurons, contributing to their degeneration and PD. While LTCC-blockers are already in clinical trials as PD-therapy, age-dependent functional roles of Cav1.3 LTCCs in SN DA neurons remain unclear. Thus, we analysed juvenile and adult Cav1.3-deficient mice with electrophysiological and molecular techniques. To unmask compensatory effects, we compared Cav1.3 KO mice with pharmacological LTCC-inhibition. LTCC-function was not necessary for SN DA pacemaker-activity at either age, but rather contributed to their pacemaker-precision. Moreover, juvenile Cav1.3 KO but not WT mice displayed adult wildtype-like, sensitised inhibitory dopamine-D2-autoreceptor (D2-AR) responses that depended upon both, interaction of the neuronal calcium sensor NCS-1 with D2-ARs, and on voltage-gated T-type calcium channel (TTCC) activity. This functional KO-phenotype was accompanied by cell-specific up-regulation of NCS-1 and Cav3.1-TTCC mRNA. Furthermore, in wildtype we identified an age-dependent switch of TTCC-function from contributing to SN DA pacemaker-precision in juveniles to pacemaker-frequency in adults. This novel interplay of Cav1.3 L-type and Cav3.1 T-type channels, and their modulation of SN DA activity-pattern and D2-AR-sensitisation, provide new insights into flexible age- and calcium-dependent activity-control of SN DA neurons and its pharmacological modulation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Poetschke</LastName><ForeName>Christina</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dragicevic</LastName><ForeName>Elena</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Duda</LastName><ForeName>Johanna</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Benkert</LastName><ForeName>Julia</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dougalis</LastName><ForeName>Antonios</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>DeZio</LastName><ForeName>Roberta</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Snutch</LastName><ForeName>Terrance P</ForeName><Initials>TP</Initials><AffiliationInfo><Affiliation>Djavad Mowafaghian Centre for Brain and Health and Michael Smith Laboratories, University of British Columbia, V6T1Z4 Vancouver, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Striessnig</LastName><ForeName>Joerg</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute of Pharmacy, Department of Pharmacology and Toxicology, University of Innsbruck, 6020 Innsbruck, Austria.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Liss</LastName><ForeName>Birgit</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Institute of Applied Physiology, University of Ulm, 89081 Ulm, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>10677</GrantID><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>09</Month><Day>18</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017660">Autoreceptors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C485995">Cacna1d protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002121">Calcium Channel Blockers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020746">Calcium Channels, L-Type</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020747">Calcium Channels, T-Type</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051580">Neuronal Calcium-Sensor 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Nigra</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4585382</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>05</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>08</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>9</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>9</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>8</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26381090</ArticleId><ArticleId IdType="pii">srep13688</ArticleId><ArticleId IdType="doi">10.1038/srep13688</ArticleId><ArticleId IdType="pmc">PMC4585382</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li><li>Autriche</li><li>Canada</li></country><region><li>Bade-Wurtemberg</li><li>District de Tübingen</li></region><settlement><li>Ulm</li></settlement><orgName><li>Université d'Ulm</li></orgName></list><tree><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Poetschke, Christina" sort="Poetschke, Christina" uniqKey="Poetschke C" first="Christina" last="Poetschke">Christina Poetschke</name></region><name sortKey="Benkert, Julia" sort="Benkert, Julia" uniqKey="Benkert J" first="Julia" last="Benkert">Julia Benkert</name><name sortKey="Dezio, Roberta" sort="Dezio, Roberta" uniqKey="Dezio R" first="Roberta" last="Dezio">Roberta Dezio</name><name sortKey="Dougalis, Antonios" sort="Dougalis, Antonios" uniqKey="Dougalis A" first="Antonios" last="Dougalis">Antonios Dougalis</name><name sortKey="Dragicevic, Elena" sort="Dragicevic, Elena" uniqKey="Dragicevic E" first="Elena" last="Dragicevic">Elena Dragicevic</name><name sortKey="Duda, Johanna" sort="Duda, Johanna" uniqKey="Duda J" first="Johanna" last="Duda">Johanna Duda</name><name sortKey="Liss, Birgit" sort="Liss, Birgit" uniqKey="Liss B" first="Birgit" last="Liss">Birgit Liss</name></country><country name="Canada"><noRegion><name sortKey="Snutch, Terrance P" sort="Snutch, Terrance P" uniqKey="Snutch T" first="Terrance P" last="Snutch">Terrance P. Snutch</name></noRegion></country><country name="Autriche"><noRegion><name sortKey="Striessnig, Joerg" sort="Striessnig, Joerg" uniqKey="Striessnig J" first="Joerg" last="Striessnig">Joerg Striessnig</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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