ParkinsonCanadaV1, Main, Exploration, bibRecord, 002095

INTERFERON-γ DEFICIENCY MODIFIES THE MOTOR AND CO-MORBID BEHAVIORAL PATHOLOGY AND NEUROCHEMICAL CHANGES PROVOKED BY THE PESTICIDE PARAQUAT

Identifieur interne : 002095 ( Main/Exploration ); précédent : 002094; suivant : 002096

INTERFERON-γ DEFICIENCY MODIFIES THE MOTOR AND CO-MORBID BEHAVIORAL PATHOLOGY AND NEUROCHEMICAL CHANGES PROVOKED BY THE PESTICIDE PARAQUAT

Auteurs : D. Litteljohn [Canada] ; E. Mangano [Canada] ; N. Shukla [Canada] ; S. Hayley [Canada]

Source :

Neuroscience [ 0306-4522 ] ; 2009.

RBID : Pascal:10-0028776

Descripteurs français

Pascal (Inist)
- Interféron gamma, Comportement, Paraquat, Cytokine, Monoamine, Dégénérescence, Maladie de Parkinson.

English descriptors

KwdEn :
- Behavior, Cytokine, Degeneration, Gamma interferon, Monoamine, Paraquat, Parkinson disease.

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-γ), 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-γ-deficient mice. Correspondingly, paraquat promoted somewhat divergent variations in neurochemical activity among wild-type and IFN-γ 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-γ 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-γ 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-γ in the striatal and motor pathology, as well as the co-morbid behavioral and hippocampal changes induced by paraquat.

Affiliations:

Canada

Links toward previous steps (curation, corpus...)

to stream PascalFrancis, to step Corpus: 000477
to stream PascalFrancis, to step Curation: 000800
to stream PascalFrancis, to step Checkpoint: 000459
to stream Main, to step Merge: 002263
to stream Main, to step Curation: 002095

Le document en format XML

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<front><div type="abstract" xml:lang="en">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-γ), 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-γ-deficient mice. Correspondingly, paraquat promoted somewhat divergent variations in neurochemical activity among wild-type and IFN-γ 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-γ 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-γ 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-γ in the striatal and motor pathology, as well as the co-morbid behavioral and hippocampal changes induced by paraquat.</div>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

INTERFERON-γ DEFICIENCY MODIFIES THE MOTOR AND CO-MORBID BEHAVIORAL PATHOLOGY AND NEUROCHEMICAL CHANGES PROVOKED BY THE PESTICIDE PARAQUAT

INTERFERON-γ DEFICIENCY MODIFIES THE MOTOR AND CO-MORBID BEHAVIORAL PATHOLOGY AND NEUROCHEMICAL CHANGES PROVOKED BY THE PESTICIDE PARAQUAT

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri