Peripheral inflammation increases the deleterious effect of CNS inflammation on the nigrostriatal dopaminergic system
► Mild peripheral inflammation exacerbates damage to dopaminergic neurons. ► The effect of peripheral inflammation is also produced without BBB disruption. ► Peripheral inflammations should be considered a risk factor for Parkinson's disease. Evidence supports the role of inflammation in the de...
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| Veröffentlicht in: | Neurotoxicology (Park Forest South) 2012-06, Vol.33 (3), p.347-360 |
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| creator | Hernández-Romero, Mª Carmen Delgado-Cortés, Mª José Sarmiento, Manuel de Pablos, Rocío M. Espinosa-Oliva, Ana María Argüelles, Sandro Bández, Manuel J. Villarán, Ruth F. Mauriño, Raquel Santiago, Marti Venero, José L. Herrera, Antonio J. Cano, Josefina Machado, Alberto |
| description | ► Mild peripheral inflammation exacerbates damage to dopaminergic neurons. ► The effect of peripheral inflammation is also produced without BBB disruption. ► Peripheral inflammations should be considered a risk factor for Parkinson's disease.
Evidence supports the role of inflammation in the development of neurodegenerative diseases. In this work, we are interested in inflammation as a risk factor by itself and not only as a factor contributing to neurodegeneration. We tested the influence of a mild to moderate peripheral inflammation (injection of carrageenan into the paws of rats) on the degeneration of dopaminergic neurons in an animal model based on the intranigral injection of lipopolysaccharide (LPS), a potent inflammatory agent. Overall, the treatment with carrageenan increased the effect of the intranigral injection of LPS on the loss of dopaminergic neurons in the SN along with all the other parameters studied, including: serum levels of the inflammatory markers TNF-α, IL-1β, IL-6 and C-reactive protein; activation of microglia, expression of proinflammatory cytokines, the adhesion molecule ICAM and the enzyme iNOS, loss of astrocytes and damage to the blood brain barrier (BBB). The possible implication of BBB rupture in the increased loss of dopaminergic neurons has been studied using another Parkinson's disease animal model based on the intraperitoneal injection of rotenone. In this experiment, loss of dopaminergic neurons was also strengthened by carrageenan, without affecting the BBB. In conclusion, our data show that a mild to moderate peripheral inflammation can exacerbate the degeneration of dopaminergic neurons caused by a harmful stimulus. |
| doi_str_mv | 10.1016/j.neuro.2012.01.018 |
| format | Article |
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Evidence supports the role of inflammation in the development of neurodegenerative diseases. In this work, we are interested in inflammation as a risk factor by itself and not only as a factor contributing to neurodegeneration. We tested the influence of a mild to moderate peripheral inflammation (injection of carrageenan into the paws of rats) on the degeneration of dopaminergic neurons in an animal model based on the intranigral injection of lipopolysaccharide (LPS), a potent inflammatory agent. Overall, the treatment with carrageenan increased the effect of the intranigral injection of LPS on the loss of dopaminergic neurons in the SN along with all the other parameters studied, including: serum levels of the inflammatory markers TNF-α, IL-1β, IL-6 and C-reactive protein; activation of microglia, expression of proinflammatory cytokines, the adhesion molecule ICAM and the enzyme iNOS, loss of astrocytes and damage to the blood brain barrier (BBB). The possible implication of BBB rupture in the increased loss of dopaminergic neurons has been studied using another Parkinson's disease animal model based on the intraperitoneal injection of rotenone. In this experiment, loss of dopaminergic neurons was also strengthened by carrageenan, without affecting the BBB. In conclusion, our data show that a mild to moderate peripheral inflammation can exacerbate the degeneration of dopaminergic neurons caused by a harmful stimulus.</description><identifier>ISSN: 0161-813X</identifier><identifier>EISSN: 1872-9711</identifier><identifier>DOI: 10.1016/j.neuro.2012.01.018</identifier><identifier>PMID: 22330755</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Activated microglia ; Animal models ; Animals ; Astrocytes ; Astrocytes - metabolism ; Astrocytes - pathology ; Basal Ganglia - metabolism ; Basal Ganglia - pathology ; Biological and medical sciences ; Blood-brain barrier ; Blood-Brain Barrier - metabolism ; Blood-Brain Barrier - pathology ; C-reactive protein ; C-Reactive Protein - metabolism ; Carrageenan ; carrageenans ; Central nervous system ; Data processing ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Disease Models, Animal ; Dopamine ; Dopamine - metabolism ; Dopaminergic neurons ; Dopaminergic Neurons - metabolism ; Dopaminergic Neurons - pathology ; Encephalitis - chemically induced ; Encephalitis - complications ; Encephalitis - metabolism ; Encephalitis - pathology ; Enzymes ; Inflammation ; Inflammation - chemically induced ; Inflammation - complications ; Inflammation - metabolism ; Inflammation - pathology ; Inflammation Mediators - blood ; Intercellular Adhesion Molecule-1 - metabolism ; Interleukin 1 ; Interleukin 6 ; Interleukin-1beta - blood ; Interleukin-6 - blood ; Lipopolysaccharide ; Lipopolysaccharides ; Male ; Medical sciences ; Movement disorders ; Nervous system (semeiology, syndromes) ; Nervous system as a whole ; Neurodegeneration ; Neurodegenerative diseases ; Neurology ; Nitric Oxide Synthase Type II - metabolism ; Nitric-oxide synthase ; Parkinson's disease ; Peripheral inflammation ; Rats ; Rats, Wistar ; Risk factors ; Rotenone ; Striatonigral Degeneration - etiology ; Striatonigral Degeneration - metabolism ; Striatonigral Degeneration - pathology ; Substantia Nigra - metabolism ; Substantia Nigra - pathology ; Time Factors ; Toxicology ; Tumor necrosis factor- alpha ; Tumor Necrosis Factor-alpha - blood</subject><ispartof>Neurotoxicology (Park Forest South), 2012-06, Vol.33 (3), p.347-360</ispartof><rights>2012 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2012 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-53c2937c04725d51d11c25bf9c9a41ef49cc1a92c6cece7e0f19164e721b48ac3</citedby><cites>FETCH-LOGICAL-c488t-53c2937c04725d51d11c25bf9c9a41ef49cc1a92c6cece7e0f19164e721b48ac3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0161813X12000332$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26011766$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22330755$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hernández-Romero, Mª Carmen</creatorcontrib><creatorcontrib>Delgado-Cortés, Mª José</creatorcontrib><creatorcontrib>Sarmiento, Manuel</creatorcontrib><creatorcontrib>de Pablos, Rocío M.</creatorcontrib><creatorcontrib>Espinosa-Oliva, Ana María</creatorcontrib><creatorcontrib>Argüelles, Sandro</creatorcontrib><creatorcontrib>Bández, Manuel J.</creatorcontrib><creatorcontrib>Villarán, Ruth F.</creatorcontrib><creatorcontrib>Mauriño, Raquel</creatorcontrib><creatorcontrib>Santiago, Marti</creatorcontrib><creatorcontrib>Venero, José L.</creatorcontrib><creatorcontrib>Herrera, Antonio J.</creatorcontrib><creatorcontrib>Cano, Josefina</creatorcontrib><creatorcontrib>Machado, Alberto</creatorcontrib><title>Peripheral inflammation increases the deleterious effect of CNS inflammation on the nigrostriatal dopaminergic system</title><title>Neurotoxicology (Park Forest South)</title><addtitle>Neurotoxicology</addtitle><description>► Mild peripheral inflammation exacerbates damage to dopaminergic neurons. ► The effect of peripheral inflammation is also produced without BBB disruption. ► Peripheral inflammations should be considered a risk factor for Parkinson's disease.
Evidence supports the role of inflammation in the development of neurodegenerative diseases. In this work, we are interested in inflammation as a risk factor by itself and not only as a factor contributing to neurodegeneration. We tested the influence of a mild to moderate peripheral inflammation (injection of carrageenan into the paws of rats) on the degeneration of dopaminergic neurons in an animal model based on the intranigral injection of lipopolysaccharide (LPS), a potent inflammatory agent. Overall, the treatment with carrageenan increased the effect of the intranigral injection of LPS on the loss of dopaminergic neurons in the SN along with all the other parameters studied, including: serum levels of the inflammatory markers TNF-α, IL-1β, IL-6 and C-reactive protein; activation of microglia, expression of proinflammatory cytokines, the adhesion molecule ICAM and the enzyme iNOS, loss of astrocytes and damage to the blood brain barrier (BBB). The possible implication of BBB rupture in the increased loss of dopaminergic neurons has been studied using another Parkinson's disease animal model based on the intraperitoneal injection of rotenone. In this experiment, loss of dopaminergic neurons was also strengthened by carrageenan, without affecting the BBB. In conclusion, our data show that a mild to moderate peripheral inflammation can exacerbate the degeneration of dopaminergic neurons caused by a harmful stimulus.</description><subject>Activated microglia</subject><subject>Animal models</subject><subject>Animals</subject><subject>Astrocytes</subject><subject>Astrocytes - metabolism</subject><subject>Astrocytes - pathology</subject><subject>Basal Ganglia - metabolism</subject><subject>Basal Ganglia - pathology</subject><subject>Biological and medical sciences</subject><subject>Blood-brain barrier</subject><subject>Blood-Brain Barrier - metabolism</subject><subject>Blood-Brain Barrier - pathology</subject><subject>C-reactive protein</subject><subject>C-Reactive Protein - metabolism</subject><subject>Carrageenan</subject><subject>carrageenans</subject><subject>Central nervous system</subject><subject>Data processing</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Disease Models, Animal</subject><subject>Dopamine</subject><subject>Dopamine - metabolism</subject><subject>Dopaminergic neurons</subject><subject>Dopaminergic Neurons - metabolism</subject><subject>Dopaminergic Neurons - pathology</subject><subject>Encephalitis - chemically induced</subject><subject>Encephalitis - complications</subject><subject>Encephalitis - metabolism</subject><subject>Encephalitis - pathology</subject><subject>Enzymes</subject><subject>Inflammation</subject><subject>Inflammation - chemically induced</subject><subject>Inflammation - complications</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Inflammation Mediators - blood</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Interleukin 1</subject><subject>Interleukin 6</subject><subject>Interleukin-1beta - blood</subject><subject>Interleukin-6 - blood</subject><subject>Lipopolysaccharide</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Movement disorders</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Nervous system as a whole</subject><subject>Neurodegeneration</subject><subject>Neurodegenerative diseases</subject><subject>Neurology</subject><subject>Nitric Oxide Synthase Type II - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Parkinson's disease</subject><subject>Peripheral inflammation</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Risk factors</subject><subject>Rotenone</subject><subject>Striatonigral Degeneration - etiology</subject><subject>Striatonigral Degeneration - metabolism</subject><subject>Striatonigral Degeneration - pathology</subject><subject>Substantia Nigra - metabolism</subject><subject>Substantia Nigra - pathology</subject><subject>Time Factors</subject><subject>Toxicology</subject><subject>Tumor necrosis factor- alpha</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><issn>0161-813X</issn><issn>1872-9711</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1rGzEQhkVoaFy3vyAQ9lLoZR2N9kO7hxyKSZuCSQJJoTchz45smf1wJG3A_z5y7aT0EnhBCJ53NHoYOwc-Aw7l5WbW0-iGmeAgZhxiqhM2gUqKtJYAH9gkUpBWkP05Y5-833AOhSzrj-xMiCzjsigmbLwnZ7drcrpNbG9a3XU62KGPF3SkPfkkrClpqKUQyWH0CRlDGJLBJPPbh_9LMXu6tys3-OCsDnFsM2x1Z3tyK4uJ3_lA3Wd2anTr6cvxnLLfP64f5zfp4u7nr_n3RYp5VYW0yFDUmUSeS1E0BTQAKIqlqbHWOZDJa0TQtcASCUkSN1BDmZMUsMwrjdmUfTvM3brhaSQfVGc9UtvqnuJXFHDBqzzLo6Mpyw4oxtW9I6O2znba7SKk9r7VRv31rfa-FYeYKrYujg-My46at86r4Ah8PQLao26N0z1a_48rOYAsy8hdHTiKOp4tOeXRUo_UWBdtq2aw7y7yAiEToes</recordid><startdate>20120601</startdate><enddate>20120601</enddate><creator>Hernández-Romero, Mª Carmen</creator><creator>Delgado-Cortés, Mª José</creator><creator>Sarmiento, Manuel</creator><creator>de Pablos, Rocío M.</creator><creator>Espinosa-Oliva, Ana María</creator><creator>Argüelles, Sandro</creator><creator>Bández, Manuel J.</creator><creator>Villarán, Ruth F.</creator><creator>Mauriño, Raquel</creator><creator>Santiago, Marti</creator><creator>Venero, José L.</creator><creator>Herrera, Antonio J.</creator><creator>Cano, Josefina</creator><creator>Machado, Alberto</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20120601</creationdate><title>Peripheral inflammation increases the deleterious effect of CNS inflammation on the nigrostriatal dopaminergic system</title><author>Hernández-Romero, Mª Carmen ; Delgado-Cortés, Mª José ; Sarmiento, Manuel ; de Pablos, Rocío M. ; Espinosa-Oliva, Ana María ; Argüelles, Sandro ; Bández, Manuel J. ; Villarán, Ruth F. ; Mauriño, Raquel ; Santiago, Marti ; Venero, José L. ; Herrera, Antonio J. ; Cano, Josefina ; Machado, Alberto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-53c2937c04725d51d11c25bf9c9a41ef49cc1a92c6cece7e0f19164e721b48ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Activated microglia</topic><topic>Animal models</topic><topic>Animals</topic><topic>Astrocytes</topic><topic>Astrocytes - metabolism</topic><topic>Astrocytes - pathology</topic><topic>Basal Ganglia - metabolism</topic><topic>Basal Ganglia - pathology</topic><topic>Biological and medical sciences</topic><topic>Blood-brain barrier</topic><topic>Blood-Brain Barrier - metabolism</topic><topic>Blood-Brain Barrier - pathology</topic><topic>C-reactive protein</topic><topic>C-Reactive Protein - metabolism</topic><topic>Carrageenan</topic><topic>carrageenans</topic><topic>Central nervous system</topic><topic>Data processing</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Disease Models, Animal</topic><topic>Dopamine</topic><topic>Dopamine - metabolism</topic><topic>Dopaminergic neurons</topic><topic>Dopaminergic Neurons - metabolism</topic><topic>Dopaminergic Neurons - pathology</topic><topic>Encephalitis - chemically induced</topic><topic>Encephalitis - complications</topic><topic>Encephalitis - metabolism</topic><topic>Encephalitis - pathology</topic><topic>Enzymes</topic><topic>Inflammation</topic><topic>Inflammation - chemically induced</topic><topic>Inflammation - complications</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Inflammation Mediators - blood</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Interleukin 1</topic><topic>Interleukin 6</topic><topic>Interleukin-1beta - blood</topic><topic>Interleukin-6 - blood</topic><topic>Lipopolysaccharide</topic><topic>Lipopolysaccharides</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Movement disorders</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Nervous system as a whole</topic><topic>Neurodegeneration</topic><topic>Neurodegenerative diseases</topic><topic>Neurology</topic><topic>Nitric Oxide Synthase Type II - metabolism</topic><topic>Nitric-oxide synthase</topic><topic>Parkinson's disease</topic><topic>Peripheral inflammation</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Risk factors</topic><topic>Rotenone</topic><topic>Striatonigral Degeneration - etiology</topic><topic>Striatonigral Degeneration - metabolism</topic><topic>Striatonigral Degeneration - pathology</topic><topic>Substantia Nigra - metabolism</topic><topic>Substantia Nigra - pathology</topic><topic>Time Factors</topic><topic>Toxicology</topic><topic>Tumor necrosis factor- alpha</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hernández-Romero, Mª Carmen</creatorcontrib><creatorcontrib>Delgado-Cortés, Mª José</creatorcontrib><creatorcontrib>Sarmiento, Manuel</creatorcontrib><creatorcontrib>de Pablos, Rocío M.</creatorcontrib><creatorcontrib>Espinosa-Oliva, Ana María</creatorcontrib><creatorcontrib>Argüelles, Sandro</creatorcontrib><creatorcontrib>Bández, Manuel J.</creatorcontrib><creatorcontrib>Villarán, Ruth F.</creatorcontrib><creatorcontrib>Mauriño, Raquel</creatorcontrib><creatorcontrib>Santiago, Marti</creatorcontrib><creatorcontrib>Venero, José L.</creatorcontrib><creatorcontrib>Herrera, Antonio J.</creatorcontrib><creatorcontrib>Cano, Josefina</creatorcontrib><creatorcontrib>Machado, Alberto</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Neurotoxicology (Park Forest South)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hernández-Romero, Mª Carmen</au><au>Delgado-Cortés, Mª José</au><au>Sarmiento, Manuel</au><au>de Pablos, Rocío M.</au><au>Espinosa-Oliva, Ana María</au><au>Argüelles, Sandro</au><au>Bández, Manuel J.</au><au>Villarán, Ruth F.</au><au>Mauriño, Raquel</au><au>Santiago, Marti</au><au>Venero, José L.</au><au>Herrera, Antonio J.</au><au>Cano, Josefina</au><au>Machado, Alberto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peripheral inflammation increases the deleterious effect of CNS inflammation on the nigrostriatal dopaminergic system</atitle><jtitle>Neurotoxicology (Park Forest South)</jtitle><addtitle>Neurotoxicology</addtitle><date>2012-06-01</date><risdate>2012</risdate><volume>33</volume><issue>3</issue><spage>347</spage><epage>360</epage><pages>347-360</pages><issn>0161-813X</issn><eissn>1872-9711</eissn><abstract>► Mild peripheral inflammation exacerbates damage to dopaminergic neurons. ► The effect of peripheral inflammation is also produced without BBB disruption. ► Peripheral inflammations should be considered a risk factor for Parkinson's disease.
Evidence supports the role of inflammation in the development of neurodegenerative diseases. In this work, we are interested in inflammation as a risk factor by itself and not only as a factor contributing to neurodegeneration. We tested the influence of a mild to moderate peripheral inflammation (injection of carrageenan into the paws of rats) on the degeneration of dopaminergic neurons in an animal model based on the intranigral injection of lipopolysaccharide (LPS), a potent inflammatory agent. Overall, the treatment with carrageenan increased the effect of the intranigral injection of LPS on the loss of dopaminergic neurons in the SN along with all the other parameters studied, including: serum levels of the inflammatory markers TNF-α, IL-1β, IL-6 and C-reactive protein; activation of microglia, expression of proinflammatory cytokines, the adhesion molecule ICAM and the enzyme iNOS, loss of astrocytes and damage to the blood brain barrier (BBB). The possible implication of BBB rupture in the increased loss of dopaminergic neurons has been studied using another Parkinson's disease animal model based on the intraperitoneal injection of rotenone. In this experiment, loss of dopaminergic neurons was also strengthened by carrageenan, without affecting the BBB. In conclusion, our data show that a mild to moderate peripheral inflammation can exacerbate the degeneration of dopaminergic neurons caused by a harmful stimulus.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>22330755</pmid><doi>10.1016/j.neuro.2012.01.018</doi><tpages>14</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Neurotoxicology (Park Forest South), 2012-06, Vol.33 (3), p.347-360 |
| issn | 0161-813X 1872-9711 |
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| subjects | Activated microglia Animal models Animals Astrocytes Astrocytes - metabolism Astrocytes - pathology Basal Ganglia - metabolism Basal Ganglia - pathology Biological and medical sciences Blood-brain barrier Blood-Brain Barrier - metabolism Blood-Brain Barrier - pathology C-reactive protein C-Reactive Protein - metabolism Carrageenan carrageenans Central nervous system Data processing Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Disease Models, Animal Dopamine Dopamine - metabolism Dopaminergic neurons Dopaminergic Neurons - metabolism Dopaminergic Neurons - pathology Encephalitis - chemically induced Encephalitis - complications Encephalitis - metabolism Encephalitis - pathology Enzymes Inflammation Inflammation - chemically induced Inflammation - complications Inflammation - metabolism Inflammation - pathology Inflammation Mediators - blood Intercellular Adhesion Molecule-1 - metabolism Interleukin 1 Interleukin 6 Interleukin-1beta - blood Interleukin-6 - blood Lipopolysaccharide Lipopolysaccharides Male Medical sciences Movement disorders Nervous system (semeiology, syndromes) Nervous system as a whole Neurodegeneration Neurodegenerative diseases Neurology Nitric Oxide Synthase Type II - metabolism Nitric-oxide synthase Parkinson's disease Peripheral inflammation Rats Rats, Wistar Risk factors Rotenone Striatonigral Degeneration - etiology Striatonigral Degeneration - metabolism Striatonigral Degeneration - pathology Substantia Nigra - metabolism Substantia Nigra - pathology Time Factors Toxicology Tumor necrosis factor- alpha Tumor Necrosis Factor-alpha - blood |
| title | Peripheral inflammation increases the deleterious effect of CNS inflammation on the nigrostriatal dopaminergic system |
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