Calcineurin/NFAT-Induced Up-Regulation of the Fas Ligand/Fas Death Pathway Is Involved in Methamphetamine-Induced Neuronal Apoptosis
Methamphetamine [METH ("speed")] is an abused psychostimulant that can cause psychotic, cognitive, and psychomotor impairment in humans. These signs and symptoms are thought to be related to dysfunctions in basal ganglionic structures of the brain. To identify possible molecular bases for...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 102; no. 3; pp. 868 - 873 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
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United States
National Academy of Sciences
18.01.2005
National Acad Sciences |
Subjects | |
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Abstract | Methamphetamine [METH ("speed")] is an abused psychostimulant that can cause psychotic, cognitive, and psychomotor impairment in humans. These signs and symptoms are thought to be related to dysfunctions in basal ganglionic structures of the brain. To identify possible molecular bases for these clinical manifestations, we first used cDNA microarray technology to measure METH-induced transcriptional responses in the striatum of rats treated with an apoptosis-inducing dose of the drug. METH injection resulted in increased expression of members of the Jun, Egr, and Nur77 subfamilies of transcription factors (TFs), changes that were confirmed by quantitative PCR. Because pathways linked to these factors are involved in the up-regulation of Fas ligand (FasL), FasL mRNA was quantified and found to be increased. Immunohistochemical studies also revealed METH-induced increased FasL protein expression in striatal GABAergic neurons that express enkephalin. Moreover, there were METH-mediated increases in calcineurin, as well as shuttling of nuclear factor of activated T cells (NFAT)c3 and NFATc4 from the cytosol to the nucleus of METH-treated rats, mechanisms also known to be involved in FasL regulation. Furthermore, METH induced cleavage of caspase-3 in FasL- and Fas-containing neurons. Finally, the METH-induced changes in the FasL-Fas death pathway were attenuated by pretreatment with the dopamine D1 receptor antagonist, SCH23390, which also caused attenuation of METH-induced apoptosis. These observations indicate that METH causes some of its neurodegenerative effects, in part, via stimulation of the Fas-mediated cell death pathway consequent to FasL up-regulation mediated by activation of multiple TFs. |
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AbstractList | Methamphetamine [METH (“speed”)] is an abused psychostimulant that can cause psychotic, cognitive, and psychomotor impairment in humans. These signs and symptoms are thought to be related to dysfunctions in basal ganglionic structures of the brain. To identify possible molecular bases for these clinical manifestations, we first used cDNA microarray technology to measure METH-induced transcriptional responses in the striatum of rats treated with an apoptosis-inducing dose of the drug. METH injection resulted in increased expression of members of the Jun, Egr, and Nur77 subfamilies of transcription factors (TFs), changes that were confirmed by quantitative PCR. Because pathways linked to these factors are involved in the up-regulation of Fas ligand (FasL), FasL mRNA was quantified and found to be increased. Immunohistochemical studies also revealed METH-induced increased FasL protein expression in striatal GABAergic neurons that express enkephalin. Moreover, there were METH-mediated increases in calcineurin, as well as shuttling of nuclear factor of activated T cells (NFAT)c3 and NFATc4 from the cytosol to the nucleus of METH-treated rats, mechanisms also known to be involved in FasL regulation. Furthermore, METH induced cleavage of caspase-3 in FasL- and Fas-containing neurons. Finally, the METH-induced changes in the FasL-Fas death pathway were attenuated by pretreatment with the dopamine D1 receptor antagonist, SCH23390, which also caused attenuation of METH-induced apoptosis. These observations indicate that METH causes some of its neurodegenerative effects, in part, via stimulation of the Fas-mediated cell death pathway consequent to FasL up-regulation mediated by activation of multiple TFs. Methamphetamine [METH ("speed")] is an abused psychostimulant that can cause psychotic, cognitive, and psychomotor impairment in humans. These signs and symptoms are thought to be related to dysfunctions in basal ganglionic structures of the brain. To identify possible molecular bases for these clinical manifestations, we first used cDNA microarray technology to measure METH-induced transcriptional responses in the striatum of rats treated with an apoptosis-inducing dose of the drug. METH injection resulted in increased expression of members of the Jun, Egr, and Nur77 subfamilies of transcription factors (TFs), changes that were confirmed by quantitative PCR. Because pathways linked to these factors are involved in the up-regulation of Fas ligand (FasL), FasL mRNA was quantified and found to be increased. Immunohistochemical studies also revealed METH-induced increased FasL protein expression in striatal GABAergic neurons that express enkephalin. Moreover, there were METH-mediated increases in calcineurin, as well as shuttling of nuclear factor of activated T cells (NFAT)c3 and NFATc4 from the cytosol to the nucleus of METH-treated rats, mechanisms also known to be involved in FasL regulation. Furthermore, METH induced cleavage of caspase-3 in FasL- and Fas-containing neurons. Finally, the METH-induced changes in the FasL-Fas death pathway were attenuated by pretreatment with the dopamine D1 receptor antagonist, SCH23390 which also caused attenuation of METH-induced apoptosis. These observations indicate that METH causes some of its neurodegenerative effects, in part, via stimulation of the Fas-mediated cell death pathway consequent to FasL up-regulation mediated by activation of multiple TFs.[PUBLICATION ABSTRACT] Methamphetamine [METH (“speed”)] is an abused psychostimulant that can cause psychotic, cognitive, and psychomotor impairment in humans. These signs and symptoms are thought to be related to dysfunctions in basal ganglionic structures of the brain. To identify possible molecular bases for these clinical manifestations, we first used cDNA microarray technology to measure METH-induced transcriptional responses in the striatum of rats treated with an apoptosis-inducing dose of the drug. METH injection resulted in increased expression of members of the Jun, Egr, and Nur77 subfamilies of transcription factors (TFs), changes that were confirmed by quantitative PCR. Because pathways linked to these factors are involved in the up-regulation of Fas ligand (FasL), FasL mRNA was quantified and found to be increased. Immunohistochemical studies also revealed METH-induced increased FasL protein expression in striatal GABAergic neurons that express enkephalin. Moreover, there were METH-mediated increases in calcineurin, as well as shuttling of nuclear factor of activated T cells (NFAT)c3 and NFATc4 from the cytosol to the nucleus of METH-treated rats, mechanisms also known to be involved in FasL regulation. Furthermore, METH induced cleavage of caspase-3 in FasL- and Fas-containing neurons. Finally, the METH-induced changes in the FasL-Fas death pathway were attenuated by pretreatment with the dopamine D1 receptor antagonist, SCH23390, which also caused attenuation of METH-induced apoptosis. These observations indicate that METH causes some of its neurodegenerative effects, in part, via stimulation of the Fas-mediated cell death pathway consequent to FasL up-regulation mediated by activation of multiple TFs. calcium neurodegeneration gelsolin Egr |
Author | Cadet, Jean Lud Hökfelt, Tomas Jayanthi, Subramaniam Ladenheim, Bruce Cai, Ning-Sheng Deng, Xiaolin McCoy, Michael T. Cluster, Andrew |
AuthorAffiliation | Molecular Neuropsychiatry Branch, National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Department of Health and Human Services, 5500 Nathan Shock Drive, Baltimore, MD 21224 |
AuthorAffiliation_xml | – name: Molecular Neuropsychiatry Branch, National Institute on Drug Abuse Intramural Research Program, National Institutes of Health, Department of Health and Human Services, 5500 Nathan Shock Drive, Baltimore, MD 21224 |
Author_xml | – sequence: 1 givenname: Subramaniam surname: Jayanthi fullname: Jayanthi, Subramaniam – sequence: 2 givenname: Xiaolin surname: Deng fullname: Deng, Xiaolin – sequence: 3 givenname: Bruce surname: Ladenheim fullname: Ladenheim, Bruce – sequence: 4 givenname: Michael T. surname: McCoy fullname: McCoy, Michael T. – sequence: 5 givenname: Andrew surname: Cluster fullname: Cluster, Andrew – sequence: 6 givenname: Ning-Sheng surname: Cai fullname: Cai, Ning-Sheng – sequence: 7 givenname: Jean Lud surname: Cadet fullname: Cadet, Jean Lud – sequence: 8 givenname: Tomas surname: Hökfelt fullname: Hökfelt, Tomas |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/15644446$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 S.J. and X.D. contributed equally to this work. Author contributions: J.L.C. designed research; S.J., X.D., B.L., M.T.M., A.C., and N.-s.C. performed research; S.J., X.D., B.L., A.C., and M.T.M. analyzed data; and S.J., X.D., and J.L.C. wrote the paper. Edited by Tomas Hökfelt, Karolinska Institutet, Stockholm, Sweden, and approved December 9, 2004 This paper was submitted directly (Track II) to the PNAS office. Abbreviations: METH, methamphetamine; DA, dopamine; TF, transcription factor; FasL, Fas ligand; ENK, enkephalin; NFAT, nuclear factor of activated T cells; SP, Substance P; GAD, glutamic acid decarboxylase; Egr, early growth response gene. To whom correspondence should be addressed. E-mail: jcadet@intra.nida.nih.gov. |
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Snippet | Methamphetamine [METH ("speed")] is an abused psychostimulant that can cause psychotic, cognitive, and psychomotor impairment in humans. These signs and... Methamphetamine [METH (“speed”)] is an abused psychostimulant that can cause psychotic, cognitive, and psychomotor impairment in humans. These signs and... |
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SubjectTerms | Active Transport, Cell Nucleus - drug effects Animals Antibodies Apoptosis Apoptosis - drug effects Biological Sciences Brain Calcineurin Calcium Cell death Cell membranes Corpus Striatum - metabolism DNA-Binding Proteins - metabolism Dosage Fas Ligand Protein fas Receptor - metabolism Male Membrane Glycoproteins - metabolism Messenger RNA Methamphetamine Methamphetamine - pharmacology Nerve Tissue Proteins - metabolism Neurology Neurons Neurons - cytology Neurons - drug effects Neurons - metabolism NFATC Transcription Factors Nuclear Proteins - metabolism Rats Rats, Sprague-Dawley T lymphocytes Transcription Factors - genetics Transcription Factors - metabolism Transcription, Genetic - drug effects Up regulation |
Title | Calcineurin/NFAT-Induced Up-Regulation of the Fas Ligand/Fas Death Pathway Is Involved in Methamphetamine-Induced Neuronal Apoptosis |
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