Cyclooxygenase‐2 deficiency modifies the neurochemical effects, motor impairment and co‐morbid anxiety provoked by paraquat administration in mice
Identifieur interne : 001213 ( Main/Corpus ); précédent : 001212; suivant : 001214Cyclooxygenase‐2 deficiency modifies the neurochemical effects, motor impairment and co‐morbid anxiety provoked by paraquat administration in mice
Auteurs : Darcy Litteljohn ; Emily N. Mangano ; Shawn HayleySource :
- European Journal of Neuroscience [ 0953-816X ] ; 2008-08.
English descriptors
- KwdEn :
Abstract
Parkinson’s disease and other motor disorders of midbrain basal ganglia dopaminergic functioning are often characterized by alterations of brainstem and limbic systems with accompanying co‐morbid anxiety and depressive symptoms. Accumulating evidence suggests that inflammatory processes may play an important role in such neurodegenerative and psychiatric pathology. In this regard, inhibition of the inflammatory enzyme cyclooxygenase‐2 (COX‐2) was reported to limit the impact of stressors as well as the neurodegenerative effects of dopaminergic toxins. The present investigation assessed the impact of the putative dopamine toxin paraquat (a widely used herbicide) upon motor functioning, behavioural indices of anxiety‐like states and central monoamine levels and whether these effects were altered in mice lacking COX‐2. Indeed, paraquat did induce motor impairment and altered dopamine utilization within the striatum, and COX‐2 deletion moderately attenuated these effects. Conversely, COX‐2 deficiency enhanced the impact of paraquat upon indices of anxiety (open field exploration) and on serotonergic, noradrenergic and dopaminergic alterations within two brain regions implicated in stressor‐related pathologies, namely the dorsal hippocampus and medial prefrontal cortex. These results suggest that COX‐2 might differentially influence the motor and psychiatric symptoms associated with environmental toxin exposure. Furthermore, these data indicate that the neurochemical impact of paraquat is not restricted to the nigrostriatal dopamine pathway but also involves stressor‐sensitive limbic regions. It is possible that COX‐2 may play a dual role by contributing to the motor impairment induced by paraquat, but acting to moderate the effects of paraquat upon processes aligned with anxiety and depression.
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DOI: 10.1111/j.1460-9568.2008.06371.x
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Accumulating evidence suggests that inflammatory processes may play an important role in such neurodegenerative and psychiatric pathology. In this regard, inhibition of the inflammatory enzyme cyclooxygenase‐2 (COX‐2) was reported to limit the impact of stressors as well as the neurodegenerative effects of dopaminergic toxins. The present investigation assessed the impact of the putative dopamine toxin paraquat (a widely used herbicide) upon motor functioning, behavioural indices of anxiety‐like states and central monoamine levels and whether these effects were altered in mice lacking COX‐2. Indeed, paraquat did induce motor impairment and altered dopamine utilization within the striatum, and COX‐2 deletion moderately attenuated these effects. Conversely, COX‐2 deficiency enhanced the impact of paraquat upon indices of anxiety (open field exploration) and on serotonergic, noradrenergic and dopaminergic alterations within two brain regions implicated in stressor‐related pathologies, namely the dorsal hippocampus and medial prefrontal cortex. These results suggest that COX‐2 might differentially influence the motor and psychiatric symptoms associated with environmental toxin exposure. Furthermore, these data indicate that the neurochemical impact of paraquat is not restricted to the nigrostriatal dopamine pathway but also involves stressor‐sensitive limbic regions. 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Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd</copyright><eventGroup><event type="firstOnline" date="2008-07-24"></event><event type="publishedOnlineFinalForm" date="2008-08-05"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-02"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="707">707</numbering><numbering type="pageLast" number="716">716</numbering></numberingGroup><correspondenceTo>Dr S. Hayley, as above.
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Litteljohn <i>et al.</i></title><title type="short">COX‐2 modulation of paraquat induced functional alterations</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>Darcy</givenNames><familyName>Litteljohn</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#aff-1-1"><personName><givenNames>Emily N.</givenNames><familyName>Mangano</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#aff-1-1"><personName><givenNames>Shawn</givenNames><familyName>Hayley</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="CA"><unparsedAffiliation>Institute of Neuroscience, Carleton University, Ottawa, ON K1S 5B6, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">co‐morbidity</keyword><keyword xml:id="k2">cytokine</keyword><keyword xml:id="k3">neurodegeneration</keyword><keyword xml:id="k4">neuroinflammatory</keyword><keyword xml:id="k5">Parkinson’s disease</keyword><keyword xml:id="k6">pesticide</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Parkinson’s disease and other motor disorders of midbrain basal ganglia dopaminergic functioning are often characterized by alterations of brainstem and limbic systems with accompanying co‐morbid anxiety and depressive symptoms. 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Accumulating evidence suggests that inflammatory processes may play an important role in such neurodegenerative and psychiatric pathology. In this regard, inhibition of the inflammatory enzyme cyclooxygenase‐2 (COX‐2) was reported to limit the impact of stressors as well as the neurodegenerative effects of dopaminergic toxins. The present investigation assessed the impact of the putative dopamine toxin paraquat (a widely used herbicide) upon motor functioning, behavioural indices of anxiety‐like states and central monoamine levels and whether these effects were altered in mice lacking COX‐2. Indeed, paraquat did induce motor impairment and altered dopamine utilization within the striatum, and COX‐2 deletion moderately attenuated these effects. Conversely, COX‐2 deficiency enhanced the impact of paraquat upon indices of anxiety (open field exploration) and on serotonergic, noradrenergic and dopaminergic alterations within two brain regions implicated in stressor‐related pathologies, namely the dorsal hippocampus and medial prefrontal cortex. These results suggest that COX‐2 might differentially influence the motor and psychiatric symptoms associated with environmental toxin exposure. Furthermore, these data indicate that the neurochemical impact of paraquat is not restricted to the nigrostriatal dopamine pathway but also involves stressor‐sensitive limbic regions. It is possible that COX‐2 may play a dual role by contributing to the motor impairment induced by paraquat, but acting to moderate the effects of paraquat upon processes aligned with anxiety and depression.</abstract><subject lang="en"><genre>Keywords</genre><topic>co‐morbidity</topic><topic>cytokine</topic><topic>neurodegeneration</topic><topic>neuroinflammatory</topic><topic>Parkinson’s disease</topic><topic>pesticide</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>707</start><end>716</end><total>10</total></extent></part></relatedItem><identifier type="istex">6C11D0CC2910B736E500A3905C4A476FBB5EAA3D</identifier><identifier type="DOI">10.1111/j.1460-9568.2008.06371.x</identifier><identifier type="ArticleID">EJN6371</identifier><accessCondition type="use and reproduction" contentType="copyright">© The Authors (2008). 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