c-fos mRNA in mouse brain after MPTP treatment
The neurotoxin, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) induces a transient increase of mRNA for the immediate-early gene c-fos in the mouse brain. The c-fos mRNA level is MPTP dose-dependent and is evident in all brain regions tested including striatum, hypothalamus, cortex, hippocampus...
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Veröffentlicht in: | Neurochemistry international 1992-04, Vol.20 (3), p.281-287 |
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creator | Duchemin, A.M. Gudehithlu, K.P. Neff, N.H. Hadjiconstantinou, M. |
description | The neurotoxin, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) induces a transient increase of mRNA for the immediate-early gene
c-fos in the mouse brain. The
c-fos mRNA level is MPTP dose-dependent and is evident in all brain regions tested including striatum, hypothalamus, cortex, hippocampus, cerebellum and midbrain. There are regional differences in the time-course for the rise of
c-fos mRNA. Pretreatment with deprenyl, a selective monoamine oxidase B inhibitor, pargyline, a nonselective monoamine oxidase inhibitor, or mazindol, a dopamine uptake transport inhibitor, does not prevent the
c-fos mRNA increase, suggesting that the elevation is due to the action of MPTP and not its neurotoxic metabolite MPP
+. |
doi_str_mv | 10.1016/0197-0186(92)90042-P |
format | Article |
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c-fos in the mouse brain. The
c-fos mRNA level is MPTP dose-dependent and is evident in all brain regions tested including striatum, hypothalamus, cortex, hippocampus, cerebellum and midbrain. There are regional differences in the time-course for the rise of
c-fos mRNA. Pretreatment with deprenyl, a selective monoamine oxidase B inhibitor, pargyline, a nonselective monoamine oxidase inhibitor, or mazindol, a dopamine uptake transport inhibitor, does not prevent the
c-fos mRNA increase, suggesting that the elevation is due to the action of MPTP and not its neurotoxic metabolite MPP
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c-fos in the mouse brain. The
c-fos mRNA level is MPTP dose-dependent and is evident in all brain regions tested including striatum, hypothalamus, cortex, hippocampus, cerebellum and midbrain. There are regional differences in the time-course for the rise of
c-fos mRNA. Pretreatment with deprenyl, a selective monoamine oxidase B inhibitor, pargyline, a nonselective monoamine oxidase inhibitor, or mazindol, a dopamine uptake transport inhibitor, does not prevent the
c-fos mRNA increase, suggesting that the elevation is due to the action of MPTP and not its neurotoxic metabolite MPP
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Psychology</topic><topic>Genes, fos</topic><topic>Kinetics</topic><topic>Male</topic><topic>Mazindol - pharmacology</topic><topic>Mice</topic><topic>Neurotoxins - pharmacology</topic><topic>Organ Specificity</topic><topic>Pargyline - pharmacology</topic><topic>Reference Values</topic><topic>RNA - isolation & purification</topic><topic>RNA, Messenger - metabolism</topic><topic>Selegiline - pharmacology</topic><topic>Time Factors</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Duchemin, A.M.</creatorcontrib><creatorcontrib>Gudehithlu, K.P.</creatorcontrib><creatorcontrib>Neff, N.H.</creatorcontrib><creatorcontrib>Hadjiconstantinou, M.</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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Neurochemistry international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Duchemin, A.M.</au><au>Gudehithlu, K.P.</au><au>Neff, N.H.</au><au>Hadjiconstantinou, M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>c-fos mRNA in mouse brain after MPTP treatment</atitle><jtitle>Neurochemistry international</jtitle><addtitle>Neurochem Int</addtitle><date>1992-04</date><risdate>1992</risdate><volume>20</volume><issue>3</issue><spage>281</spage><epage>287</epage><pages>281-287</pages><issn>0197-0186</issn><eissn>1872-9754</eissn><coden>NEUIDS</coden><abstract>The neurotoxin, MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) induces a transient increase of mRNA for the immediate-early gene
c-fos in the mouse brain. The
c-fos mRNA level is MPTP dose-dependent and is evident in all brain regions tested including striatum, hypothalamus, cortex, hippocampus, cerebellum and midbrain. There are regional differences in the time-course for the rise of
c-fos mRNA. Pretreatment with deprenyl, a selective monoamine oxidase B inhibitor, pargyline, a nonselective monoamine oxidase inhibitor, or mazindol, a dopamine uptake transport inhibitor, does not prevent the
c-fos mRNA increase, suggesting that the elevation is due to the action of MPTP and not its neurotoxic metabolite MPP
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subjects | 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine - pharmacology Animals Biochemistry and metabolism Biological and medical sciences Blotting, Northern Brain - drug effects Brain - metabolism Central nervous system Dose-Response Relationship, Drug Fundamental and applied biological sciences. Psychology Genes, fos Kinetics Male Mazindol - pharmacology Mice Neurotoxins - pharmacology Organ Specificity Pargyline - pharmacology Reference Values RNA - isolation & purification RNA, Messenger - metabolism Selegiline - pharmacology Time Factors Vertebrates: nervous system and sense organs |
title | c-fos mRNA in mouse brain after MPTP treatment |
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