Bilateral upregulation of α-synuclein expression in the mouse substantia nigra by intracranial rotenone treatment.
Identifieur interne : 000120 ( Main/Exploration ); précédent : 000119; suivant : 000121Bilateral upregulation of α-synuclein expression in the mouse substantia nigra by intracranial rotenone treatment.
Auteurs : Candace H. Carriere [Canada] ; Na Hyea Kang [Canada] ; Lennard P. Niles [Canada]Source :
- Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie [ 1618-1433 ] ; 2017.
English descriptors
- KwdEn :
- Animals, Disease Models, Animal, Immunohistochemistry, Injections, Intraventricular, Insecticides (administration & dosage), Insecticides (toxicity), Male, Mice, Parkinson Disease (physiopathology), Rotenone (administration & dosage), Rotenone (toxicity), Substantia Nigra (drug effects), Substantia Nigra (pathology), Up-Regulation, alpha-Synuclein (biosynthesis).
- MESH :
- chemical , administration & dosage : Insecticides, Rotenone.
- chemical , biosynthesis : alpha-Synuclein.
- chemical , toxicity : Insecticides, Rotenone.
- drug effects : Substantia Nigra.
- pathology : Substantia Nigra.
- physiopathology : Parkinson Disease.
- Animals, Disease Models, Animal, Immunohistochemistry, Injections, Intraventricular, Male, Mice, Up-Regulation.
Abstract
The pesticide rotenone has been shown to cause systemic inhibition of mitochondrial complex I activity, with consequent degeneration of dopamine neurons along the nigrostriatal pathway, as observed in Parkinson's disease (PD). Recently, intracranial infusion of rotenone was found to increase the protein levels of the Lewy body constituents, α-synuclein and small ubiquitin-related modifier-1(SUMO-1), in the lesioned hemisphere of the mouse brain. These findings are supportive of a mouse model of PD, but information about the dopamine-synthesizing enzyme, tyrosine hydroxylase (TH), an essential marker of dopaminergic status, was not reported. Clarification of this issue is important because an intracranial rotenone mouse model of Parkinson's disease has not been established. Towards this end, the present study examined the effects of intracranial rotenone treatment on TH and α-synuclein immunohistochemistry in addition to forelimb motor function. Mice were unilaterally infused with either vehicle or rotenone (2μg/site) in both the medial forebrain bundle and the substantia nigra. The forelimb asymmetry (cylinder) test indicated a significant decrease in use of the contralateral forelimb in lesioned animals as compared to the sham group. Densitometric analysis revealed a significant depletion of TH immunofluorescence within the ipsilateral striatum and substantia nigra of lesioned animals. Moreover, a significant bilateral increase in α-synuclein immunofluorescence was found in the substantia nigra of lesioned mice, as compared to control animals. These findings indicate that this intracranial rotenone mouse model will be useful for studies of neurodegenerative disorders such as PD.
DOI: 10.1016/j.etp.2016.12.007
PubMed: 27986376
Affiliations:
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Le document en format XML
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Carriere</name><affiliation wicri:level="4"><nlm:affiliation>Department of Psychiatry and Behavioural Neurosciences, Faculty of Health Sciences, McMaster University, 1200 Main Street West, Hamilton, ON, L8N 3Z5, Canada. Electronic address: candace.carriere@gmail.com.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Psychiatry and Behavioural Neurosciences, Faculty of Health Sciences, McMaster University, 1200 Main Street West, Hamilton, ON, L8N 3Z5</wicri:regionArea><orgName type="university">Université McMaster</orgName><placeName><settlement type="city">Hamilton (Ontario)</settlement><region type="state">Ontario</region></placeName></affiliation></author><author><name sortKey="Kang, Na Hyea" sort="Kang, Na Hyea" uniqKey="Kang N" first="Na Hyea" last="Kang">Na Hyea Kang</name><affiliation wicri:level="4"><nlm:affiliation>Department of Psychiatry and Behavioural Neurosciences, Faculty of Health Sciences, McMaster University, 1200 Main Street West, Hamilton, ON, L8N 3Z5, Canada. Electronic address: rachel.nh.kang@gmail.com.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Psychiatry and Behavioural Neurosciences, Faculty of Health Sciences, McMaster University, 1200 Main Street West, Hamilton, ON, L8N 3Z5</wicri:regionArea><orgName type="university">Université McMaster</orgName><placeName><settlement type="city">Hamilton (Ontario)</settlement><region type="state">Ontario</region></placeName></affiliation></author><author><name sortKey="Niles, Lennard P" sort="Niles, Lennard P" uniqKey="Niles L" first="Lennard P" last="Niles">Lennard P. Niles</name><affiliation wicri:level="4"><nlm:affiliation>Department of Psychiatry and Behavioural Neurosciences, Faculty of Health Sciences, McMaster University, 1200 Main Street West, Hamilton, ON, L8N 3Z5, Canada. Electronic address: niles@mcmaster.ca.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Psychiatry and Behavioural Neurosciences, Faculty of Health Sciences, McMaster University, 1200 Main Street West, Hamilton, ON, L8N 3Z5</wicri:regionArea><orgName type="university">Université McMaster</orgName><placeName><settlement type="city">Hamilton (Ontario)</settlement><region type="state">Ontario</region></placeName></affiliation></author></analytic><series><title level="j">Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie</title><idno type="eISSN">1618-1433</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Immunohistochemistry</term><term>Injections, Intraventricular</term><term>Insecticides (administration & dosage)</term><term>Insecticides (toxicity)</term><term>Male</term><term>Mice</term><term>Parkinson Disease (physiopathology)</term><term>Rotenone (administration & dosage)</term><term>Rotenone (toxicity)</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (pathology)</term><term>Up-Regulation</term><term>alpha-Synuclein (biosynthesis)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Insecticides</term><term>Rotenone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Insecticides</term><term>Rotenone</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Immunohistochemistry</term><term>Injections, Intraventricular</term><term>Male</term><term>Mice</term><term>Up-Regulation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The pesticide rotenone has been shown to cause systemic inhibition of mitochondrial complex I activity, with consequent degeneration of dopamine neurons along the nigrostriatal pathway, as observed in Parkinson's disease (PD). Recently, intracranial infusion of rotenone was found to increase the protein levels of the Lewy body constituents, α-synuclein and small ubiquitin-related modifier-1(SUMO-1), in the lesioned hemisphere of the mouse brain. These findings are supportive of a mouse model of PD, but information about the dopamine-synthesizing enzyme, tyrosine hydroxylase (TH), an essential marker of dopaminergic status, was not reported. Clarification of this issue is important because an intracranial rotenone mouse model of Parkinson's disease has not been established. Towards this end, the present study examined the effects of intracranial rotenone treatment on TH and α-synuclein immunohistochemistry in addition to forelimb motor function. Mice were unilaterally infused with either vehicle or rotenone (2μg/site) in both the medial forebrain bundle and the substantia nigra. The forelimb asymmetry (cylinder) test indicated a significant decrease in use of the contralateral forelimb in lesioned animals as compared to the sham group. Densitometric analysis revealed a significant depletion of TH immunofluorescence within the ipsilateral striatum and substantia nigra of lesioned animals. Moreover, a significant bilateral increase in α-synuclein immunofluorescence was found in the substantia nigra of lesioned mice, as compared to control animals. These findings indicate that this intracranial rotenone mouse model will be useful for studies of neurodegenerative disorders such as PD.</div></front></TEI><affiliations><list><country><li>Canada</li></country><region><li>Ontario</li></region><settlement><li>Hamilton (Ontario)</li></settlement><orgName><li>Université McMaster</li></orgName></list><tree><country name="Canada"><region name="Ontario"><name sortKey="Carriere, Candace H" sort="Carriere, Candace H" uniqKey="Carriere C" first="Candace H" last="Carriere">Candace H. Carriere</name></region><name sortKey="Kang, Na Hyea" sort="Kang, Na Hyea" uniqKey="Kang N" first="Na Hyea" last="Kang">Na Hyea Kang</name><name sortKey="Niles, Lennard P" sort="Niles, Lennard P" uniqKey="Niles L" first="Lennard P" last="Niles">Lennard P. Niles</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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