Region-specific transcriptional response to chronic nicotine in rat brain
Even though nicotine has been shown to modulate mRNA expression of a variety of genes, a comprehensive high-throughput study of the effects of nicotine on the tissue-specific gene expression profiles has been lacking in the literature. In this study, cDNA microarrays containing 1117 genes and ESTs w...
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| Veröffentlicht in: | Brain research 2001-08, Vol.909 (1), p.194-203 |
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| creator | Konu, Özlen Kane, Justin K Barrett, Tanya Vawter, Marquis P Chang, Ruying Ma, Jennie Z Donovan, David M Sharp, Burt Becker, Kevin G Li, Ming D |
| description | Even though nicotine has been shown to modulate mRNA expression of a variety of genes, a comprehensive high-throughput study of the effects of nicotine on the tissue-specific gene expression profiles has been lacking in the literature. In this study, cDNA microarrays containing 1117 genes and ESTs were used to assess the transcriptional response to chronic nicotine treatment in rat, based on four brain regions, i.e. prefrontal cortex (PFC), nucleus accumbens (NAs), ventral tegmental area (VTA), and amygdala (AMYG). On the basis of a non-parametric resampling method, an index (called jackknifed reliability index, JRI) was proposed, and employed to determine the inherent measurement error across multiple arrays used in this study. Upon removal of the outliers, the mean correlation coefficient between duplicate measurements increased to 0.978±0.0035 from 0.941±0.045. Results from principal component analysis and pairwise correlations suggested that brain regions studied were highly similar in terms of their absolute expression levels, but exhibited divergent transcriptional responses to chronic nicotine administration. For example, PFC and NAs were significantly more similar to each other (
r=0.7;
P |
| doi_str_mv | 10.1016/S0006-8993(01)02685-3 |
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r=0.7;
P<10
−14) than to either VTA or AMYG. Furthermore, we confirmed our microarray results for two representative genes, i.e. the weak inward rectifier K
+ channel (TWIK-1), and phosphate and tensin homolog (PTEN) by using real-time quantitative RT-PCR technique. Finally, a number of genes, involved in MAPK, phosphatidylinositol, and EGFR signaling pathways, were identified and proposed as possible targets in response to nicotine administration.</description><identifier>ISSN: 0006-8993</identifier><identifier>EISSN: 1872-6240</identifier><identifier>DOI: 10.1016/S0006-8993(01)02685-3</identifier><identifier>PMID: 11478936</identifier><identifier>CODEN: BRREAP</identifier><language>eng</language><publisher>London: Elsevier B.V</publisher><subject>Amygdala - drug effects ; Amygdala - metabolism ; Animals ; Biological and medical sciences ; Brain ; Brain - drug effects ; Brain - metabolism ; Drug Administration Schedule ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - physiology ; Genes - drug effects ; Genes - physiology ; Male ; Medical sciences ; Microarray ; mRNA expression ; Nicotine ; Nicotine - pharmacology ; Nicotinic Agonists - pharmacology ; Normalization ; Nucleus Accumbens - drug effects ; Nucleus Accumbens - metabolism ; Oligonucleotide Array Sequence Analysis ; Pathway ; Phosphoric Monoester Hydrolases - drug effects ; Phosphoric Monoester Hydrolases - metabolism ; Potassium Channels - drug effects ; Potassium Channels - metabolism ; Potassium Channels, Tandem Pore Domain ; Prefrontal Cortex - drug effects ; Prefrontal Cortex - metabolism ; PTEN Phosphohydrolase ; Rats ; Rats, Sprague-Dawley ; Reproducibility of Results ; RNA, Messenger - drug effects ; RNA, Messenger - metabolism ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Tobacco Use Disorder - genetics ; Tobacco Use Disorder - metabolism ; Tobacco Use Disorder - physiopathology ; Tobacco, tobacco smoking ; Toxicology ; Transcription, Genetic - drug effects ; Transcription, Genetic - physiology ; Tumor Suppressor Proteins ; ventral tegmental area ; Ventral Tegmental Area - drug effects ; Ventral Tegmental Area - metabolism</subject><ispartof>Brain research, 2001-08, Vol.909 (1), p.194-203</ispartof><rights>2001 Elsevier Science B.V.</rights><rights>2002 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c605t-6bd89bd47ea8b3bee4ff9016bfb7ba545f782e3b7f43c7bda07637a1406b807b3</citedby><cites>FETCH-LOGICAL-c605t-6bd89bd47ea8b3bee4ff9016bfb7ba545f782e3b7f43c7bda07637a1406b807b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0006-8993(01)02685-3$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14093102$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11478936$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Konu, Özlen</creatorcontrib><creatorcontrib>Kane, Justin K</creatorcontrib><creatorcontrib>Barrett, Tanya</creatorcontrib><creatorcontrib>Vawter, Marquis P</creatorcontrib><creatorcontrib>Chang, Ruying</creatorcontrib><creatorcontrib>Ma, Jennie Z</creatorcontrib><creatorcontrib>Donovan, David M</creatorcontrib><creatorcontrib>Sharp, Burt</creatorcontrib><creatorcontrib>Becker, Kevin G</creatorcontrib><creatorcontrib>Li, Ming D</creatorcontrib><title>Region-specific transcriptional response to chronic nicotine in rat brain</title><title>Brain research</title><addtitle>Brain Res</addtitle><description>Even though nicotine has been shown to modulate mRNA expression of a variety of genes, a comprehensive high-throughput study of the effects of nicotine on the tissue-specific gene expression profiles has been lacking in the literature. In this study, cDNA microarrays containing 1117 genes and ESTs were used to assess the transcriptional response to chronic nicotine treatment in rat, based on four brain regions, i.e. prefrontal cortex (PFC), nucleus accumbens (NAs), ventral tegmental area (VTA), and amygdala (AMYG). On the basis of a non-parametric resampling method, an index (called jackknifed reliability index, JRI) was proposed, and employed to determine the inherent measurement error across multiple arrays used in this study. Upon removal of the outliers, the mean correlation coefficient between duplicate measurements increased to 0.978±0.0035 from 0.941±0.045. Results from principal component analysis and pairwise correlations suggested that brain regions studied were highly similar in terms of their absolute expression levels, but exhibited divergent transcriptional responses to chronic nicotine administration. For example, PFC and NAs were significantly more similar to each other (
r=0.7;
P<10
−14) than to either VTA or AMYG. Furthermore, we confirmed our microarray results for two representative genes, i.e. the weak inward rectifier K
+ channel (TWIK-1), and phosphate and tensin homolog (PTEN) by using real-time quantitative RT-PCR technique. Finally, a number of genes, involved in MAPK, phosphatidylinositol, and EGFR signaling pathways, were identified and proposed as possible targets in response to nicotine administration.</description><subject>Amygdala - drug effects</subject><subject>Amygdala - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain - drug effects</subject><subject>Brain - metabolism</subject><subject>Drug Administration Schedule</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - physiology</subject><subject>Genes - drug effects</subject><subject>Genes - physiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microarray</subject><subject>mRNA expression</subject><subject>Nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Nicotinic Agonists - pharmacology</subject><subject>Normalization</subject><subject>Nucleus Accumbens - drug effects</subject><subject>Nucleus Accumbens - metabolism</subject><subject>Oligonucleotide Array Sequence Analysis</subject><subject>Pathway</subject><subject>Phosphoric Monoester Hydrolases - drug effects</subject><subject>Phosphoric Monoester Hydrolases - metabolism</subject><subject>Potassium Channels - drug effects</subject><subject>Potassium Channels - metabolism</subject><subject>Potassium Channels, Tandem Pore Domain</subject><subject>Prefrontal Cortex - drug effects</subject><subject>Prefrontal Cortex - metabolism</subject><subject>PTEN Phosphohydrolase</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reproducibility of Results</subject><subject>RNA, Messenger - drug effects</subject><subject>RNA, Messenger - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Tobacco Use Disorder - genetics</subject><subject>Tobacco Use Disorder - metabolism</subject><subject>Tobacco Use Disorder - physiopathology</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><subject>Transcription, Genetic - drug effects</subject><subject>Transcription, Genetic - physiology</subject><subject>Tumor Suppressor Proteins</subject><subject>ventral tegmental area</subject><subject>Ventral Tegmental Area - drug effects</subject><subject>Ventral Tegmental Area - metabolism</subject><issn>0006-8993</issn><issn>1872-6240</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFvFSEUhUmjaV-rP6HNbDS6GL0MDDAbjWmqNmnSpOqaAHNpaebBFOY18d9L-15aXbkgBPjuuZdzCDmm8IECFR9_AIBo1TCwd0DfQydU37I9sqJKdq3oOLwgqyfkgByWcluPjA2wTw4o5VINTKzI-RVehxTbMqMLPrhmySYWl8O81GszNRnLnGLBZkmNu8kpVqautISITYhNNktjswnxFXnpzVTw9W4_Ir--nv08_d5eXH47P_1y0ToB_dIKO6rBjlyiUZZZRO79UD9kvZXW9Lz3UnXIrPScOWlHA1IwaSgHYRVIy47Ip63uvLFrHB3GOvKk5xzWJv_WyQT970sMN_o63WsGg-olVIG3O4Gc7jZYFr0OxeE0mYhpUzRVoCjjsoL9FnQ5lZLRPzWhoB9C0I8h6AeHNVD9GIJmte7k7wmfq3auV-DNDjDFmclXy10ozxyHgVHoKvd5y2H18z5g1sUFjA7HkNEtekzhP6P8AdUopho</recordid><startdate>20010803</startdate><enddate>20010803</enddate><creator>Konu, Özlen</creator><creator>Kane, Justin K</creator><creator>Barrett, Tanya</creator><creator>Vawter, Marquis P</creator><creator>Chang, Ruying</creator><creator>Ma, Jennie Z</creator><creator>Donovan, David M</creator><creator>Sharp, Burt</creator><creator>Becker, Kevin G</creator><creator>Li, Ming D</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>5PM</scope></search><sort><creationdate>20010803</creationdate><title>Region-specific transcriptional response to chronic nicotine in rat brain</title><author>Konu, Özlen ; Kane, Justin K ; Barrett, Tanya ; Vawter, Marquis P ; Chang, Ruying ; Ma, Jennie Z ; Donovan, David M ; Sharp, Burt ; Becker, Kevin G ; Li, Ming D</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c605t-6bd89bd47ea8b3bee4ff9016bfb7ba545f782e3b7f43c7bda07637a1406b807b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Amygdala - drug effects</topic><topic>Amygdala - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Brain - drug effects</topic><topic>Brain - metabolism</topic><topic>Drug Administration Schedule</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - physiology</topic><topic>Genes - drug effects</topic><topic>Genes - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microarray</topic><topic>mRNA expression</topic><topic>Nicotine</topic><topic>Nicotine - pharmacology</topic><topic>Nicotinic Agonists - pharmacology</topic><topic>Normalization</topic><topic>Nucleus Accumbens - drug effects</topic><topic>Nucleus Accumbens - metabolism</topic><topic>Oligonucleotide Array Sequence Analysis</topic><topic>Pathway</topic><topic>Phosphoric Monoester Hydrolases - drug effects</topic><topic>Phosphoric Monoester Hydrolases - metabolism</topic><topic>Potassium Channels - drug effects</topic><topic>Potassium Channels - metabolism</topic><topic>Potassium Channels, Tandem Pore Domain</topic><topic>Prefrontal Cortex - drug effects</topic><topic>Prefrontal Cortex - metabolism</topic><topic>PTEN Phosphohydrolase</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reproducibility of Results</topic><topic>RNA, Messenger - drug effects</topic><topic>RNA, Messenger - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Tobacco Use Disorder - genetics</topic><topic>Tobacco Use Disorder - metabolism</topic><topic>Tobacco Use Disorder - physiopathology</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><topic>Transcription, Genetic - drug effects</topic><topic>Transcription, Genetic - physiology</topic><topic>Tumor Suppressor Proteins</topic><topic>ventral tegmental area</topic><topic>Ventral Tegmental Area - drug effects</topic><topic>Ventral Tegmental Area - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Konu, Özlen</creatorcontrib><creatorcontrib>Kane, Justin K</creatorcontrib><creatorcontrib>Barrett, Tanya</creatorcontrib><creatorcontrib>Vawter, Marquis P</creatorcontrib><creatorcontrib>Chang, Ruying</creatorcontrib><creatorcontrib>Ma, Jennie Z</creatorcontrib><creatorcontrib>Donovan, David M</creatorcontrib><creatorcontrib>Sharp, Burt</creatorcontrib><creatorcontrib>Becker, Kevin G</creatorcontrib><creatorcontrib>Li, Ming D</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>PubMed Central (Full Participant titles)</collection><jtitle>Brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Konu, Özlen</au><au>Kane, Justin K</au><au>Barrett, Tanya</au><au>Vawter, Marquis P</au><au>Chang, Ruying</au><au>Ma, Jennie Z</au><au>Donovan, David M</au><au>Sharp, Burt</au><au>Becker, Kevin G</au><au>Li, Ming D</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Region-specific transcriptional response to chronic nicotine in rat brain</atitle><jtitle>Brain research</jtitle><addtitle>Brain Res</addtitle><date>2001-08-03</date><risdate>2001</risdate><volume>909</volume><issue>1</issue><spage>194</spage><epage>203</epage><pages>194-203</pages><issn>0006-8993</issn><eissn>1872-6240</eissn><coden>BRREAP</coden><abstract>Even though nicotine has been shown to modulate mRNA expression of a variety of genes, a comprehensive high-throughput study of the effects of nicotine on the tissue-specific gene expression profiles has been lacking in the literature. In this study, cDNA microarrays containing 1117 genes and ESTs were used to assess the transcriptional response to chronic nicotine treatment in rat, based on four brain regions, i.e. prefrontal cortex (PFC), nucleus accumbens (NAs), ventral tegmental area (VTA), and amygdala (AMYG). On the basis of a non-parametric resampling method, an index (called jackknifed reliability index, JRI) was proposed, and employed to determine the inherent measurement error across multiple arrays used in this study. Upon removal of the outliers, the mean correlation coefficient between duplicate measurements increased to 0.978±0.0035 from 0.941±0.045. Results from principal component analysis and pairwise correlations suggested that brain regions studied were highly similar in terms of their absolute expression levels, but exhibited divergent transcriptional responses to chronic nicotine administration. For example, PFC and NAs were significantly more similar to each other (
r=0.7;
P<10
−14) than to either VTA or AMYG. Furthermore, we confirmed our microarray results for two representative genes, i.e. the weak inward rectifier K
+ channel (TWIK-1), and phosphate and tensin homolog (PTEN) by using real-time quantitative RT-PCR technique. Finally, a number of genes, involved in MAPK, phosphatidylinositol, and EGFR signaling pathways, were identified and proposed as possible targets in response to nicotine administration.</abstract><cop>London</cop><cop>Amsterdam</cop><cop>New York, NY</cop><pub>Elsevier B.V</pub><pmid>11478936</pmid><doi>10.1016/S0006-8993(01)02685-3</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amygdala - drug effects Amygdala - metabolism Animals Biological and medical sciences Brain Brain - drug effects Brain - metabolism Drug Administration Schedule Gene Expression Regulation - drug effects Gene Expression Regulation - physiology Genes - drug effects Genes - physiology Male Medical sciences Microarray mRNA expression Nicotine Nicotine - pharmacology Nicotinic Agonists - pharmacology Normalization Nucleus Accumbens - drug effects Nucleus Accumbens - metabolism Oligonucleotide Array Sequence Analysis Pathway Phosphoric Monoester Hydrolases - drug effects Phosphoric Monoester Hydrolases - metabolism Potassium Channels - drug effects Potassium Channels - metabolism Potassium Channels, Tandem Pore Domain Prefrontal Cortex - drug effects Prefrontal Cortex - metabolism PTEN Phosphohydrolase Rats Rats, Sprague-Dawley Reproducibility of Results RNA, Messenger - drug effects RNA, Messenger - metabolism Signal Transduction - drug effects Signal Transduction - physiology Tobacco Use Disorder - genetics Tobacco Use Disorder - metabolism Tobacco Use Disorder - physiopathology Tobacco, tobacco smoking Toxicology Transcription, Genetic - drug effects Transcription, Genetic - physiology Tumor Suppressor Proteins ventral tegmental area Ventral Tegmental Area - drug effects Ventral Tegmental Area - metabolism |
| title | Region-specific transcriptional response to chronic nicotine in rat brain |
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