Interferon-gamma deficiency modifies the motor and co-morbid behavioral pathology and neurochemical changes provoked by the pesticide paraquat.
Identifieur interne : 000E45 ( PubMed/Checkpoint ); précédent : 000E44; suivant : 000E46Interferon-gamma deficiency modifies the motor and co-morbid behavioral pathology and neurochemical changes provoked by the pesticide paraquat.
Auteurs : D. Litteljohn ; E. Mangano ; N. Shukla ; S. HayleySource :
- Neuroscience [ 1873-7544 ] ; 2009.
English descriptors
- KwdEn :
- Animals, Behavior, Animal (drug effects), Brain (metabolism), Dopamine (metabolism), Interferon-gamma (genetics), Mice, Mice, Knockout, Motor Activity (drug effects), Paraquat (toxicity), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (metabolism), Parkinson Disease, Secondary (psychology), Pesticides (toxicity).
- MESH :
- chemical , genetics : Interferon-gamma.
- chemical , metabolism : Dopamine.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Behavior, Animal, Motor Activity.
- metabolism : Brain, Parkinson Disease, Secondary.
- psychology : Parkinson Disease, Secondary.
- chemical , toxicity : Paraquat, Pesticides.
- Animals, Mice, Mice, Knockout.
Abstract
In addition to nigrostriatal pathology and corresponding motor disturbances, Parkinson's disease (PD) is often characterized by co-morbid neuropsychiatric symptoms, most notably anxiety and depression. Separate lines of evidence indicate that inflammatory processes associated with microglial activation and cytokine release may be fundamental to the progression of both PD and its co-morbid psychiatric pathology. Accordingly, we assessed the contribution of the pro-inflammatory cytokine, interferon-gamma (IFN-gamma), to a range of PD-like pathology provoked by the ecologically relevant herbicide and dopamine (DA) toxin, paraquat. To this end, paraquat provoked overt motor impairment (reduced home-cage activity and impaired vertical climbing) and signs of anxiety-like behavior (reduced open field exploration) in wild-type but not IFN-gamma-deficient mice. Correspondingly, paraquat promoted somewhat divergent variations in neurochemical activity among wild-type and IFN-gamma null mice at brain sites important for both motor (striatum) and co-morbid affective pathologies (dorsal hippocampus, medial prefrontal cortex, and locus coeruleus). Specifically, the herbicide provoked a dosing regimen-dependent reduction in striatal DA levels that was prevented by IFN-gamma deficiency. In addition, the herbicide influenced serotonergic and noradrenergic activity within the dorsal hippocampus and medial prefrontal cortex; and elevated noradrenergic activity within the locus coeruleus. Although genetic ablation of IFN-gamma had relatively few effects on monoamine variations within the locus coeruleus and prefrontal cortex, loss of the pro-inflammatory cytokine did normalize the paraquat-induced noradrenergic alterations within the hippocampus. These findings further elucidate the functional implications of paraquat intoxication and suggest an important role for IFN-gamma in the striatal and motor pathology, as well as the co-morbid behavioral and hippocampal changes induced by paraquat.
DOI: 10.1016/j.neuroscience.2009.09.025
PubMed: 19782123
Affiliations:
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Litteljohn</name><affiliation><nlm:affiliation>Institute of Neuroscience, Carleton University, Life Sciences Research Building, 1125 Colonel By Drive, Ottawa, ON K1S 5B6 Canada.</nlm:affiliation><wicri:noCountry code="subField">ON K1S 5B6 Canada</wicri:noCountry></affiliation></author><author><name sortKey="Mangano, E" sort="Mangano, E" uniqKey="Mangano E" first="E" last="Mangano">E. Mangano</name></author><author><name sortKey="Shukla, N" sort="Shukla, N" uniqKey="Shukla N" first="N" last="Shukla">N. Shukla</name></author><author><name sortKey="Hayley, S" sort="Hayley, S" uniqKey="Hayley S" first="S" last="Hayley">S. 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Separate lines of evidence indicate that inflammatory processes associated with microglial activation and cytokine release may be fundamental to the progression of both PD and its co-morbid psychiatric pathology. Accordingly, we assessed the contribution of the pro-inflammatory cytokine, interferon-gamma (IFN-gamma), to a range of PD-like pathology provoked by the ecologically relevant herbicide and dopamine (DA) toxin, paraquat. To this end, paraquat provoked overt motor impairment (reduced home-cage activity and impaired vertical climbing) and signs of anxiety-like behavior (reduced open field exploration) in wild-type but not IFN-gamma-deficient mice. Correspondingly, paraquat promoted somewhat divergent variations in neurochemical activity among wild-type and IFN-gamma null mice at brain sites important for both motor (striatum) and co-morbid affective pathologies (dorsal hippocampus, medial prefrontal cortex, and locus coeruleus). Specifically, the herbicide provoked a dosing regimen-dependent reduction in striatal DA levels that was prevented by IFN-gamma deficiency. In addition, the herbicide influenced serotonergic and noradrenergic activity within the dorsal hippocampus and medial prefrontal cortex; and elevated noradrenergic activity within the locus coeruleus. Although genetic ablation of IFN-gamma had relatively few effects on monoamine variations within the locus coeruleus and prefrontal cortex, loss of the pro-inflammatory cytokine did normalize the paraquat-induced noradrenergic alterations within the hippocampus. These findings further elucidate the functional implications of paraquat intoxication and suggest an important role for IFN-gamma in the striatal and motor pathology, as well as the co-morbid behavioral and hippocampal changes induced by paraquat.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19782123</PMID><DateCreated><Year>2009</Year><Month>11</Month><Day>16</Day></DateCreated><DateCompleted><Year>2010</Year><Month>02</Month><Day>19</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-7544</ISSN><JournalIssue CitedMedium="Internet"><Volume>164</Volume><Issue>4</Issue><PubDate><Year>2009</Year><Month>Dec</Month><Day>29</Day></PubDate></JournalIssue><Title>Neuroscience</Title><ISOAbbreviation>Neuroscience</ISOAbbreviation></Journal><ArticleTitle>Interferon-gamma deficiency modifies the motor and co-morbid behavioral pathology and neurochemical changes provoked by the pesticide paraquat.</ArticleTitle><Pagination><MedlinePgn>1894-906</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.neuroscience.2009.09.025</ELocationID><Abstract><AbstractText>In addition to nigrostriatal pathology and corresponding motor disturbances, Parkinson's disease (PD) is often characterized by co-morbid neuropsychiatric symptoms, most notably anxiety and depression. Separate lines of evidence indicate that inflammatory processes associated with microglial activation and cytokine release may be fundamental to the progression of both PD and its co-morbid psychiatric pathology. Accordingly, we assessed the contribution of the pro-inflammatory cytokine, interferon-gamma (IFN-gamma), to a range of PD-like pathology provoked by the ecologically relevant herbicide and dopamine (DA) toxin, paraquat. To this end, paraquat provoked overt motor impairment (reduced home-cage activity and impaired vertical climbing) and signs of anxiety-like behavior (reduced open field exploration) in wild-type but not IFN-gamma-deficient mice. Correspondingly, paraquat promoted somewhat divergent variations in neurochemical activity among wild-type and IFN-gamma null mice at brain sites important for both motor (striatum) and co-morbid affective pathologies (dorsal hippocampus, medial prefrontal cortex, and locus coeruleus). Specifically, the herbicide provoked a dosing regimen-dependent reduction in striatal DA levels that was prevented by IFN-gamma deficiency. In addition, the herbicide influenced serotonergic and noradrenergic activity within the dorsal hippocampus and medial prefrontal cortex; and elevated noradrenergic activity within the locus coeruleus. Although genetic ablation of IFN-gamma had relatively few effects on monoamine variations within the locus coeruleus and prefrontal cortex, loss of the pro-inflammatory cytokine did normalize the paraquat-induced noradrenergic alterations within the hippocampus. These findings further elucidate the functional implications of paraquat intoxication and suggest an important role for IFN-gamma in the striatal and motor pathology, as well as the co-morbid behavioral and hippocampal changes induced by paraquat.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Litteljohn</LastName><ForeName>D</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Institute of Neuroscience, Carleton University, Life Sciences Research Building, 1125 Colonel By Drive, Ottawa, ON K1S 5B6 Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mangano</LastName><ForeName>E</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Shukla</LastName><ForeName>N</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Hayley</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><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>2009</Year><Month>09</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Neuroscience</MedlineTA><NlmUniqueID>7605074</NlmUniqueID><ISSNLinking>0306-4522</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010575">Pesticides</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical><Chemical><RegistryNumber>PLG39H7695</RegistryNumber><NameOfSubstance UI="D010269">Paraquat</NameOfSubstance></Chemical><Chemical><RegistryNumber>VTD58H1Z2X</RegistryNumber><NameOfSubstance UI="D004298">Dopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001522" MajorTopicYN="N">Behavior, Animal</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004298" MajorTopicYN="N">Dopamine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007371" MajorTopicYN="N">Interferon-gamma</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009043" MajorTopicYN="N">Motor Activity</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010269" MajorTopicYN="N">Paraquat</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000523" MajorTopicYN="Y">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010575" MajorTopicYN="N">Pesticides</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2009</Year><Month>07</Month><Day>20</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2009</Year><Month>09</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>9</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>9</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>2</Month><Day>20</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19782123</ArticleId><ArticleId IdType="pii">S0306-4522(09)01500-0</ArticleId><ArticleId IdType="doi">10.1016/j.neuroscience.2009.09.025</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Hayley, S" sort="Hayley, S" uniqKey="Hayley S" first="S" last="Hayley">S. Hayley</name><name sortKey="Litteljohn, D" sort="Litteljohn, D" uniqKey="Litteljohn D" first="D" last="Litteljohn">D. Litteljohn</name><name sortKey="Mangano, E" sort="Mangano, E" uniqKey="Mangano E" first="E" last="Mangano">E. Mangano</name><name sortKey="Shukla, N" sort="Shukla, N" uniqKey="Shukla N" first="N" last="Shukla">N. Shukla</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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