Chemogenetic ablation of dopaminergic neurons leads to transient locomotor impairments in zebrafish larvae.
Identifieur interne : 000399 ( PubMed/Corpus ); précédent : 000398; suivant : 000400Chemogenetic ablation of dopaminergic neurons leads to transient locomotor impairments in zebrafish larvae.
Auteurs : Rafael Godoy ; Sandra Noble ; Kevin Yoon ; Hymie Anisman ; Marc EkkerSource :
- Journal of neurochemistry [ 1471-4159 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Animals, Genetically Modified, Brain (cytology), Brain (growth & development), Dopaminergic Neurons (drug effects), Dyskinesia, Drug-Induced (genetics), Dyskinesia, Drug-Induced (physiopathology), Green Fluorescent Proteins, Humans, Larva (growth & development), Locomotion (drug effects), MPTP Poisoning (pathology), Metronidazole (pharmacology), Nerve Regeneration, Swimming, Zebrafish.
- MESH :
- chemical , pharmacology : Metronidazole.
- chemical : Green Fluorescent Proteins.
- cytology : Brain.
- drug effects : Dopaminergic Neurons, Locomotion.
- genetics : Dyskinesia, Drug-Induced.
- growth & development : Brain, Larva.
- pathology : MPTP Poisoning.
- physiopathology : Dyskinesia, Drug-Induced.
- Animals, Animals, Genetically Modified, Humans, Nerve Regeneration, Swimming, Zebrafish.
Abstract
To determine the impact of a controlled loss of dopaminergic neurons on locomotor function, we generated transgenic zebrafish, Tg(dat:CFP-NTR), expressing a cyan fluorescent protein-nitroreductase fusion protein (CFP-NTR) under the control of dopamine transporter (dat) cis-regulatory elements. Embryonic and larval zebrafish express the transgene in several groups of dopaminergic neurons, notably in the olfactory bulb, telencephalon, diencephalon and caudal hypothalamus. Administration of the pro-drug metronidazole (Mtz) resulted in activation of caspase 3 in CFP-positive neurons and in a reduction in dat-positive cells by 5 days post-fertilization (dpf). Loss of neurons coincided with impairments in global locomotor parameters such as swimming distance, percentage of time spent moving, as well as changes in tail bend parameters such as time to maximal bend and angular velocity. Dopamine levels were transiently decreased following Mtz administration. Recovery of some of the locomotor parameters was observed by 7 dpf. However, the total numbers of dat-expressing neurons were still decreased at 7, 12, or 14 dpf, even though there was evidence for production of new dat-expressing cells. Tg(dat:CFP-NTR) zebrafish provide a model to correlate altered dopaminergic neuron numbers with locomotor function and to investigate factors influencing regeneration of dopaminergic neurons.
DOI: 10.1111/jnc.13214
PubMed: 26118896
Links to Exploration step
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Chemogenetic ablation of dopaminergic neurons leads to transient locomotor impairments in zebrafish larvae.</title><author><name sortKey="Godoy, Rafael" sort="Godoy, Rafael" uniqKey="Godoy R" first="Rafael" last="Godoy">Rafael Godoy</name><affiliation><nlm:affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Noble, Sandra" sort="Noble, Sandra" uniqKey="Noble S" first="Sandra" last="Noble">Sandra Noble</name><affiliation><nlm:affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Yoon, Kevin" sort="Yoon, Kevin" uniqKey="Yoon K" first="Kevin" last="Yoon">Kevin Yoon</name><affiliation><nlm:affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name><affiliation><nlm:affiliation>Department of Neuroscience, Carleton University, Ottawa, K1S-5B6, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Ekker, Marc" sort="Ekker, Marc" uniqKey="Ekker M" first="Marc" last="Ekker">Marc Ekker</name><affiliation><nlm:affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:26118896</idno><idno type="pmid">26118896</idno><idno type="doi">10.1111/jnc.13214</idno><idno type="wicri:Area/PubMed/Corpus">000399</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000399</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Chemogenetic ablation of dopaminergic neurons leads to transient locomotor impairments in zebrafish larvae.</title><author><name sortKey="Godoy, Rafael" sort="Godoy, Rafael" uniqKey="Godoy R" first="Rafael" last="Godoy">Rafael Godoy</name><affiliation><nlm:affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Noble, Sandra" sort="Noble, Sandra" uniqKey="Noble S" first="Sandra" last="Noble">Sandra Noble</name><affiliation><nlm:affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Yoon, Kevin" sort="Yoon, Kevin" uniqKey="Yoon K" first="Kevin" last="Yoon">Kevin Yoon</name><affiliation><nlm:affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name><affiliation><nlm:affiliation>Department of Neuroscience, Carleton University, Ottawa, K1S-5B6, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Ekker, Marc" sort="Ekker, Marc" uniqKey="Ekker M" first="Marc" last="Ekker">Marc Ekker</name><affiliation><nlm:affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of neurochemistry</title><idno type="eISSN">1471-4159</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Animals, Genetically Modified</term><term>Brain (cytology)</term><term>Brain (growth & development)</term><term>Dopaminergic Neurons (drug effects)</term><term>Dyskinesia, Drug-Induced (genetics)</term><term>Dyskinesia, Drug-Induced (physiopathology)</term><term>Green Fluorescent Proteins</term><term>Humans</term><term>Larva (growth & development)</term><term>Locomotion (drug effects)</term><term>MPTP Poisoning (pathology)</term><term>Metronidazole (pharmacology)</term><term>Nerve Regeneration</term><term>Swimming</term><term>Zebrafish</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Metronidazole</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Green Fluorescent Proteins</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Dopaminergic Neurons</term><term>Locomotion</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Brain</term><term>Larva</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>MPTP Poisoning</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Animals, Genetically Modified</term><term>Humans</term><term>Nerve Regeneration</term><term>Swimming</term><term>Zebrafish</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To determine the impact of a controlled loss of dopaminergic neurons on locomotor function, we generated transgenic zebrafish, Tg(dat:CFP-NTR), expressing a cyan fluorescent protein-nitroreductase fusion protein (CFP-NTR) under the control of dopamine transporter (dat) cis-regulatory elements. Embryonic and larval zebrafish express the transgene in several groups of dopaminergic neurons, notably in the olfactory bulb, telencephalon, diencephalon and caudal hypothalamus. Administration of the pro-drug metronidazole (Mtz) resulted in activation of caspase 3 in CFP-positive neurons and in a reduction in dat-positive cells by 5 days post-fertilization (dpf). Loss of neurons coincided with impairments in global locomotor parameters such as swimming distance, percentage of time spent moving, as well as changes in tail bend parameters such as time to maximal bend and angular velocity. Dopamine levels were transiently decreased following Mtz administration. Recovery of some of the locomotor parameters was observed by 7 dpf. However, the total numbers of dat-expressing neurons were still decreased at 7, 12, or 14 dpf, even though there was evidence for production of new dat-expressing cells. Tg(dat:CFP-NTR) zebrafish provide a model to correlate altered dopaminergic neuron numbers with locomotor function and to investigate factors influencing regeneration of dopaminergic neurons.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26118896</PMID><DateCreated><Year>2015</Year><Month>10</Month><Day>10</Day></DateCreated><DateCompleted><Year>2016</Year><Month>01</Month><Day>11</Day></DateCompleted><DateRevised><Year>2015</Year><Month>10</Month><Day>10</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1471-4159</ISSN><JournalIssue CitedMedium="Internet"><Volume>135</Volume><Issue>2</Issue><PubDate><Year>2015</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Journal of neurochemistry</Title><ISOAbbreviation>J. Neurochem.</ISOAbbreviation></Journal><ArticleTitle>Chemogenetic ablation of dopaminergic neurons leads to transient locomotor impairments in zebrafish larvae.</ArticleTitle><Pagination><MedlinePgn>249-60</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/jnc.13214</ELocationID><Abstract><AbstractText>To determine the impact of a controlled loss of dopaminergic neurons on locomotor function, we generated transgenic zebrafish, Tg(dat:CFP-NTR), expressing a cyan fluorescent protein-nitroreductase fusion protein (CFP-NTR) under the control of dopamine transporter (dat) cis-regulatory elements. Embryonic and larval zebrafish express the transgene in several groups of dopaminergic neurons, notably in the olfactory bulb, telencephalon, diencephalon and caudal hypothalamus. Administration of the pro-drug metronidazole (Mtz) resulted in activation of caspase 3 in CFP-positive neurons and in a reduction in dat-positive cells by 5 days post-fertilization (dpf). Loss of neurons coincided with impairments in global locomotor parameters such as swimming distance, percentage of time spent moving, as well as changes in tail bend parameters such as time to maximal bend and angular velocity. Dopamine levels were transiently decreased following Mtz administration. Recovery of some of the locomotor parameters was observed by 7 dpf. However, the total numbers of dat-expressing neurons were still decreased at 7, 12, or 14 dpf, even though there was evidence for production of new dat-expressing cells. Tg(dat:CFP-NTR) zebrafish provide a model to correlate altered dopaminergic neuron numbers with locomotor function and to investigate factors influencing regeneration of dopaminergic neurons.</AbstractText><CopyrightInformation>© 2015 International Society for Neurochemistry.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Godoy</LastName><ForeName>Rafael</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Noble</LastName><ForeName>Sandra</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yoon</LastName><ForeName>Kevin</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anisman</LastName><ForeName>Hymie</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Neuroscience, Carleton University, Ottawa, K1S-5B6, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ekker</LastName><ForeName>Marc</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Center for Advanced Research in Environmental Genomics, Department of Biology, University of Ottawa, Ottawa, K1N-6N5, Canada.</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>2015</Year><Month>08</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neurochem</MedlineTA><NlmUniqueID>2985190R</NlmUniqueID><ISSNLinking>0022-3042</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C485182">Cyan Fluorescent Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>140QMO216E</RegistryNumber><NameOfSubstance UI="D008795">Metronidazole</NameOfSubstance></Chemical><Chemical><RegistryNumber>147336-22-9</RegistryNumber><NameOfSubstance UI="D049452">Green Fluorescent Proteins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D030801" MajorTopicYN="N">Animals, Genetically Modified</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059290" MajorTopicYN="N">Dopaminergic Neurons</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004409" MajorTopicYN="N">Dyskinesia, Drug-Induced</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049452" MajorTopicYN="N">Green Fluorescent Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007814" MajorTopicYN="N">Larva</DescriptorName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008124" MajorTopicYN="N">Locomotion</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020267" MajorTopicYN="N">MPTP Poisoning</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008795" MajorTopicYN="N">Metronidazole</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009416" MajorTopicYN="N">Nerve Regeneration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013550" MajorTopicYN="N">Swimming</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015027" MajorTopicYN="N">Zebrafish</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">dopamine</Keyword><Keyword MajorTopicYN="N">neurodegeneration</Keyword><Keyword MajorTopicYN="N">parkinson's disease</Keyword><Keyword MajorTopicYN="N">regeneration</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>03</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>05</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>05</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>6</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>6</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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