Brain apoptosis signaling pathways are regulated by methylphenidate treatment in young and adult rats
Abstract Methylphenidate (MPH) is commonly prescribed for children who have been diagnosed with attention deficit hyperactivity disorder (ADHD); however, the action mechanisms of methylphenidate have not been fully elucidated. Studies have shown a relationship between apoptosis signaling pathways an...
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creator | Réus, Gislaine Z Scaini, Giselli Jeremias, Gabriela C Furlanetto, Camila B Morais, Meline O.S Mello-Santos, Lis Maira Quevedo, João Streck, Emilio L |
description | Abstract Methylphenidate (MPH) is commonly prescribed for children who have been diagnosed with attention deficit hyperactivity disorder (ADHD); however, the action mechanisms of methylphenidate have not been fully elucidated. Studies have shown a relationship between apoptosis signaling pathways and psychiatric disorders, as well as in therapeutic targets for such disorders. So, we investigated if chronic treatment with MPH at doses of 1, 2 and 10 mg/kg could alter the levels of pro-apoptotic protein, Bax, anti-apoptotic protein, Bcl-2, caspase-3 and cytochrome c in the brain of young and adult Wistar rats. Our results showed that MPH at all doses increased Bax in the cortex; the Bcl-2 and caspase-3 were increased with MPH (1 mg/kg) and were reduced with MPH (2 and 10 mg/kg); the cytochrome c was reduced in the cortex after treatment with MPH at all doses; in the cerebellum there was an increase of Bax with MPH at all doses, however, there was a reduction of Bcl-2, caspase-3, and cytochrome c with MPH (2 and 10 mg/kg); in the striatum the treatment with MPH (10 mg/kg) decreased caspase-3 and cytochrome c; treatment with MPH (2 and 10 mg/kg) increased Bax and decreased Bcl-2 in the hippocampus; and the caspase-3 and cytochrome c were reduced in the hippocampus with MPH (10 mg/kg). In conclusion, our results suggest that MPH influences plasticity in the brain of young and adult rats; however, the effects were dependent of age and brain area, on the one hand activating the initial cascade of apoptosis, increasing Bax and reducing Bcl-2, but otherwise inhibiting apoptosis by reduction of caspase-3 and cytochrome c. |
doi_str_mv | 10.1016/j.brainres.2014.08.010 |
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Studies have shown a relationship between apoptosis signaling pathways and psychiatric disorders, as well as in therapeutic targets for such disorders. So, we investigated if chronic treatment with MPH at doses of 1, 2 and 10 mg/kg could alter the levels of pro-apoptotic protein, Bax, anti-apoptotic protein, Bcl-2, caspase-3 and cytochrome c in the brain of young and adult Wistar rats. Our results showed that MPH at all doses increased Bax in the cortex; the Bcl-2 and caspase-3 were increased with MPH (1 mg/kg) and were reduced with MPH (2 and 10 mg/kg); the cytochrome c was reduced in the cortex after treatment with MPH at all doses; in the cerebellum there was an increase of Bax with MPH at all doses, however, there was a reduction of Bcl-2, caspase-3, and cytochrome c with MPH (2 and 10 mg/kg); in the striatum the treatment with MPH (10 mg/kg) decreased caspase-3 and cytochrome c; treatment with MPH (2 and 10 mg/kg) increased Bax and decreased Bcl-2 in the hippocampus; and the caspase-3 and cytochrome c were reduced in the hippocampus with MPH (10 mg/kg). In conclusion, our results suggest that MPH influences plasticity in the brain of young and adult rats; however, the effects were dependent of age and brain area, on the one hand activating the initial cascade of apoptosis, increasing Bax and reducing Bcl-2, but otherwise inhibiting apoptosis by reduction of caspase-3 and cytochrome c.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/j.brainres.2014.08.010</identifier><identifier>PMID: 25128604</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Animals ; Apoptosis - drug effects ; Apoptosis - physiology ; Bax ; Bcl-2 ; bcl-2-Associated X Protein - metabolism ; Biological and medical sciences ; Brain - drug effects ; Brain - growth & development ; Brain - physiology ; Caspase 3 - metabolism ; Caspase-3 ; Central Nervous System Stimulants - pharmacology ; Central Nervous System Stimulants - toxicity ; Cytochrome c ; Cytochromes c - metabolism ; Dose-Response Relationship, Drug ; Fundamental and applied biological sciences. Psychology ; Immunoblotting ; Medical sciences ; Methylphenidate ; Methylphenidate - pharmacology ; Methylphenidate - toxicity ; Neurology ; Neuropharmacology ; Neuroprotective Agents - pharmacology ; Pharmacology. Drug treatments ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer ; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) ; Psychology. Psychoanalysis. Psychiatry ; Psychopharmacology ; Rats, Wistar ; Signal Transduction - drug effects ; Vertebrates: nervous system and sense organs</subject><ispartof>Brain research, 2014-10, Vol.1583, p.269-276</ispartof><rights>Elsevier B.V.</rights><rights>2014 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2014 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-80af5ce2545b06df360d06badd227cfd36715ed0fbb7e932d9a336f440e99ea23</citedby><cites>FETCH-LOGICAL-c486t-80af5ce2545b06df360d06badd227cfd36715ed0fbb7e932d9a336f440e99ea23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainres.2014.08.010$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=28789547$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25128604$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Réus, Gislaine Z</creatorcontrib><creatorcontrib>Scaini, Giselli</creatorcontrib><creatorcontrib>Jeremias, Gabriela C</creatorcontrib><creatorcontrib>Furlanetto, Camila B</creatorcontrib><creatorcontrib>Morais, Meline O.S</creatorcontrib><creatorcontrib>Mello-Santos, Lis Maira</creatorcontrib><creatorcontrib>Quevedo, João</creatorcontrib><creatorcontrib>Streck, Emilio L</creatorcontrib><title>Brain apoptosis signaling pathways are regulated by methylphenidate treatment in young and adult rats</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Abstract Methylphenidate (MPH) is commonly prescribed for children who have been diagnosed with attention deficit hyperactivity disorder (ADHD); however, the action mechanisms of methylphenidate have not been fully elucidated. Studies have shown a relationship between apoptosis signaling pathways and psychiatric disorders, as well as in therapeutic targets for such disorders. So, we investigated if chronic treatment with MPH at doses of 1, 2 and 10 mg/kg could alter the levels of pro-apoptotic protein, Bax, anti-apoptotic protein, Bcl-2, caspase-3 and cytochrome c in the brain of young and adult Wistar rats. Our results showed that MPH at all doses increased Bax in the cortex; the Bcl-2 and caspase-3 were increased with MPH (1 mg/kg) and were reduced with MPH (2 and 10 mg/kg); the cytochrome c was reduced in the cortex after treatment with MPH at all doses; in the cerebellum there was an increase of Bax with MPH at all doses, however, there was a reduction of Bcl-2, caspase-3, and cytochrome c with MPH (2 and 10 mg/kg); in the striatum the treatment with MPH (10 mg/kg) decreased caspase-3 and cytochrome c; treatment with MPH (2 and 10 mg/kg) increased Bax and decreased Bcl-2 in the hippocampus; and the caspase-3 and cytochrome c were reduced in the hippocampus with MPH (10 mg/kg). In conclusion, our results suggest that MPH influences plasticity in the brain of young and adult rats; however, the effects were dependent of age and brain area, on the one hand activating the initial cascade of apoptosis, increasing Bax and reducing Bcl-2, but otherwise inhibiting apoptosis by reduction of caspase-3 and cytochrome c.</description><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Bax</subject><subject>Bcl-2</subject><subject>bcl-2-Associated X Protein - metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain - drug effects</subject><subject>Brain - growth & development</subject><subject>Brain - physiology</subject><subject>Caspase 3 - metabolism</subject><subject>Caspase-3</subject><subject>Central Nervous System Stimulants - pharmacology</subject><subject>Central Nervous System Stimulants - toxicity</subject><subject>Cytochrome c</subject><subject>Cytochromes c - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Immunoblotting</subject><subject>Medical sciences</subject><subject>Methylphenidate</subject><subject>Methylphenidate - pharmacology</subject><subject>Methylphenidate - toxicity</subject><subject>Neurology</subject><subject>Neuropharmacology</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer</subject><subject>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopharmacology</subject><subject>Rats, Wistar</subject><subject>Signal Transduction - drug effects</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkk9v1DAQxSMEotvCV6h8QeKSxX8Sx74gaAUFqRIH4GxN7Mmul2wSbAeUb4-j3YLEpSfL1u-9Gc-borhmdMsok28O2zaAHwLGLaes2lK1pYw-KTZMNbyUvKJPiw2lVJZKa3FRXMZ4yFchNH1eXPCacSVptSnwZrUhMI1TGqOPJPrdAL0fdmSCtP8NSyQQkATczT0kdKRdyBHTfumnPQ7e5TeSAkI64pBItlrGOYthcATc3CcSIMUXxbMO-ogvz-dV8f3jh2-3n8r7L3efb9_fl7ZSMpWKQldb5HVVt1S6TkjqqGzBOc4b2zkhG1ajo13bNqgFdxqEkF1VUdQagYur4vXJdwrjzxljMkcfLfY9DDjO0TAptFZcC_U4WuchClazFZUn1IYxxoCdmYI_QlgMo2ZNwxzMQxpmTcNQZXIaWXh9rjG3R3R_ZQ_jz8CrMwDRQt8FGKyP_zjVKF1XTebenTjMw_vlMZhoPQ4WnQ9ok3Gjf7yXt_9Z2Jyyz1V_4ILxMM4h557_bSI31Hxdd2ddHVZldVNp8Qf1WcIi</recordid><startdate>20141002</startdate><enddate>20141002</enddate><creator>Réus, Gislaine Z</creator><creator>Scaini, Giselli</creator><creator>Jeremias, Gabriela C</creator><creator>Furlanetto, Camila B</creator><creator>Morais, Meline O.S</creator><creator>Mello-Santos, Lis Maira</creator><creator>Quevedo, João</creator><creator>Streck, Emilio L</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>7X8</scope><scope>7TK</scope></search><sort><creationdate>20141002</creationdate><title>Brain apoptosis signaling pathways are regulated by methylphenidate treatment in young and adult rats</title><author>Réus, Gislaine Z ; Scaini, Giselli ; Jeremias, Gabriela C ; Furlanetto, Camila B ; Morais, Meline O.S ; Mello-Santos, Lis Maira ; Quevedo, João ; Streck, Emilio L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-80af5ce2545b06df360d06badd227cfd36715ed0fbb7e932d9a336f440e99ea23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Bax</topic><topic>Bcl-2</topic><topic>bcl-2-Associated X Protein - metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain - drug effects</topic><topic>Brain - growth & development</topic><topic>Brain - physiology</topic><topic>Caspase 3 - metabolism</topic><topic>Caspase-3</topic><topic>Central Nervous System Stimulants - pharmacology</topic><topic>Central Nervous System Stimulants - toxicity</topic><topic>Cytochrome c</topic><topic>Cytochromes c - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Immunoblotting</topic><topic>Medical sciences</topic><topic>Methylphenidate</topic><topic>Methylphenidate - pharmacology</topic><topic>Methylphenidate - toxicity</topic><topic>Neurology</topic><topic>Neuropharmacology</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer</topic><topic>Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease)</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopharmacology</topic><topic>Rats, Wistar</topic><topic>Signal Transduction - drug effects</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Réus, Gislaine Z</creatorcontrib><creatorcontrib>Scaini, Giselli</creatorcontrib><creatorcontrib>Jeremias, Gabriela C</creatorcontrib><creatorcontrib>Furlanetto, Camila B</creatorcontrib><creatorcontrib>Morais, Meline O.S</creatorcontrib><creatorcontrib>Mello-Santos, Lis Maira</creatorcontrib><creatorcontrib>Quevedo, João</creatorcontrib><creatorcontrib>Streck, Emilio L</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>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Réus, Gislaine Z</au><au>Scaini, Giselli</au><au>Jeremias, Gabriela C</au><au>Furlanetto, Camila B</au><au>Morais, Meline O.S</au><au>Mello-Santos, Lis Maira</au><au>Quevedo, João</au><au>Streck, Emilio L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Brain apoptosis signaling pathways are regulated by methylphenidate treatment in young and adult rats</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2014-10-02</date><risdate>2014</risdate><volume>1583</volume><spage>269</spage><epage>276</epage><pages>269-276</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Abstract Methylphenidate (MPH) is commonly prescribed for children who have been diagnosed with attention deficit hyperactivity disorder (ADHD); however, the action mechanisms of methylphenidate have not been fully elucidated. Studies have shown a relationship between apoptosis signaling pathways and psychiatric disorders, as well as in therapeutic targets for such disorders. So, we investigated if chronic treatment with MPH at doses of 1, 2 and 10 mg/kg could alter the levels of pro-apoptotic protein, Bax, anti-apoptotic protein, Bcl-2, caspase-3 and cytochrome c in the brain of young and adult Wistar rats. Our results showed that MPH at all doses increased Bax in the cortex; the Bcl-2 and caspase-3 were increased with MPH (1 mg/kg) and were reduced with MPH (2 and 10 mg/kg); the cytochrome c was reduced in the cortex after treatment with MPH at all doses; in the cerebellum there was an increase of Bax with MPH at all doses, however, there was a reduction of Bcl-2, caspase-3, and cytochrome c with MPH (2 and 10 mg/kg); in the striatum the treatment with MPH (10 mg/kg) decreased caspase-3 and cytochrome c; treatment with MPH (2 and 10 mg/kg) increased Bax and decreased Bcl-2 in the hippocampus; and the caspase-3 and cytochrome c were reduced in the hippocampus with MPH (10 mg/kg). In conclusion, our results suggest that MPH influences plasticity in the brain of young and adult rats; however, the effects were dependent of age and brain area, on the one hand activating the initial cascade of apoptosis, increasing Bax and reducing Bcl-2, but otherwise inhibiting apoptosis by reduction of caspase-3 and cytochrome c.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>25128604</pmid><doi>10.1016/j.brainres.2014.08.010</doi><tpages>8</tpages></addata></record> |
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subjects | Animals Apoptosis - drug effects Apoptosis - physiology Bax Bcl-2 bcl-2-Associated X Protein - metabolism Biological and medical sciences Brain - drug effects Brain - growth & development Brain - physiology Caspase 3 - metabolism Caspase-3 Central Nervous System Stimulants - pharmacology Central Nervous System Stimulants - toxicity Cytochrome c Cytochromes c - metabolism Dose-Response Relationship, Drug Fundamental and applied biological sciences. Psychology Immunoblotting Medical sciences Methylphenidate Methylphenidate - pharmacology Methylphenidate - toxicity Neurology Neuropharmacology Neuroprotective Agents - pharmacology Pharmacology. Drug treatments Proto-Oncogene Proteins c-bcl-2 - metabolism Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease) Psychology. Psychoanalysis. Psychiatry Psychopharmacology Rats, Wistar Signal Transduction - drug effects Vertebrates: nervous system and sense organs |
title | Brain apoptosis signaling pathways are regulated by methylphenidate treatment in young and adult rats |
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