Cellular mechanisms of nicotine addiction
In developed countries, tobacco use is estimated to be the largest single cause of premature death [Lancet 339 (1992) 1268]. Nicotine is the main addictive component of tobacco that motivates continued use despite the harmful effects. Nicotinic acetylcholine receptors (nAChRs) are widely distributed...
Gespeichert in:
| Veröffentlicht in: | Pharmacology, biochemistry and behavior biochemistry and behavior, 2001-12, Vol.70 (4), p.439-446 |
|---|---|
| Hauptverfasser: | , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 446 |
|---|---|
| container_issue | 4 |
| container_start_page | 439 |
| container_title | Pharmacology, biochemistry and behavior |
| container_volume | 70 |
| creator | Dani, John A. De Biasi, Mariella |
| description | In developed countries, tobacco use is estimated to be the largest single cause of premature death [Lancet 339 (1992) 1268]. Nicotine is the main addictive component of tobacco that motivates continued use despite the harmful effects. Nicotinic acetylcholine receptors (nAChRs) are widely distributed throughout the mammalian central nervous system (CNS), where they normally respond to acetylcholine (ACh) and modulate neuronal excitability and synaptic communication. Nicotinic receptors are structurally diverse and have varied roles. Presynaptic and preterminal nAChRs enhance neurotransmitter release. Postsynaptic and somal nAChRs mediate a small proportion of fast excitatory transmission and modulate cytoplasmic second messenger systems. Although the impact of nicotine obtained from tobacco is not completely understood, a portion of nicotine's addictive power is attributable to actions upon the dopaminergic systems, which normally help to reinforce rewarding behaviors. As obtained from tobacco, nicotine activates and desensitizes nAChRs, and both processes contribute to the cellular events that underlie nicotine addiction. |
| doi_str_mv | 10.1016/S0091-3057(01)00652-9 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_18256509</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0091305701006529</els_id><sourcerecordid>18256509</sourcerecordid><originalsourceid>FETCH-LOGICAL-c444t-6c5433f73904be83b061681c60fdc00fc069fd8ee2a6337354b5818e9178e9ef3</originalsourceid><addsrcrecordid>eNqFkMlKxEAQhhtRnHH0EZScxDlEq9JbchIZ3GDAg3pukk41tmTR7ozg25tZ0KOXqsv31_IxdopwiYDq6hmgwJSD1BeAcwAls7TYY1PMNU8lar3Ppr_IhB3F-A4AIlP6kE0QdaFQ8CmbL6hpVk0ZkpbsW9n52Makd0nnbT_4jpKyrr0dfN8dswNXNpFOdn3GXu9uXxYP6fLp_nFxs0ytEGJIlZWCc6d5AaKinFegUOVoFbjaAjgLqnB1TpSVinPNpahkjjkVqMdCjs_Y-XbuR-g_VxQH0_poxyvLjvpVNJhnUkkoRlBuQRv6GAM58xF8W4Zvg2DWjszGkVkLMIBm48isc2e7BauqpfovtZMyAtdbgMY3vzwFE62nzlLtA9nB1L3_Z8UPdeR0Xg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>18256509</pqid></control><display><type>article</type><title>Cellular mechanisms of nicotine addiction</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Dani, John A. ; De Biasi, Mariella</creator><creatorcontrib>Dani, John A. ; De Biasi, Mariella</creatorcontrib><description>In developed countries, tobacco use is estimated to be the largest single cause of premature death [Lancet 339 (1992) 1268]. Nicotine is the main addictive component of tobacco that motivates continued use despite the harmful effects. Nicotinic acetylcholine receptors (nAChRs) are widely distributed throughout the mammalian central nervous system (CNS), where they normally respond to acetylcholine (ACh) and modulate neuronal excitability and synaptic communication. Nicotinic receptors are structurally diverse and have varied roles. Presynaptic and preterminal nAChRs enhance neurotransmitter release. Postsynaptic and somal nAChRs mediate a small proportion of fast excitatory transmission and modulate cytoplasmic second messenger systems. Although the impact of nicotine obtained from tobacco is not completely understood, a portion of nicotine's addictive power is attributable to actions upon the dopaminergic systems, which normally help to reinforce rewarding behaviors. As obtained from tobacco, nicotine activates and desensitizes nAChRs, and both processes contribute to the cellular events that underlie nicotine addiction.</description><identifier>ISSN: 0091-3057</identifier><identifier>EISSN: 1873-5177</identifier><identifier>DOI: 10.1016/S0091-3057(01)00652-9</identifier><identifier>PMID: 11796143</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acetylcholine ; Animals ; Cigarettes ; Dopamine ; Humans ; Neurons - drug effects ; Neurons - metabolism ; Neurons - physiology ; Nicotine - pharmacology ; Nicotinic Agonists - pharmacology ; Nicotinic receptor ; Postsynaptic ; Presynaptic ; Receptors, Nicotinic - physiology ; Reinforcement ; Reward ; Smoking ; Substance-Related Disorders - metabolism ; Synaptic plasticity ; Tobacco ; Tolerance</subject><ispartof>Pharmacology, biochemistry and behavior, 2001-12, Vol.70 (4), p.439-446</ispartof><rights>2001 Elsevier Science Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c444t-6c5433f73904be83b061681c60fdc00fc069fd8ee2a6337354b5818e9178e9ef3</citedby><cites>FETCH-LOGICAL-c444t-6c5433f73904be83b061681c60fdc00fc069fd8ee2a6337354b5818e9178e9ef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0091305701006529$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11796143$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dani, John A.</creatorcontrib><creatorcontrib>De Biasi, Mariella</creatorcontrib><title>Cellular mechanisms of nicotine addiction</title><title>Pharmacology, biochemistry and behavior</title><addtitle>Pharmacol Biochem Behav</addtitle><description>In developed countries, tobacco use is estimated to be the largest single cause of premature death [Lancet 339 (1992) 1268]. Nicotine is the main addictive component of tobacco that motivates continued use despite the harmful effects. Nicotinic acetylcholine receptors (nAChRs) are widely distributed throughout the mammalian central nervous system (CNS), where they normally respond to acetylcholine (ACh) and modulate neuronal excitability and synaptic communication. Nicotinic receptors are structurally diverse and have varied roles. Presynaptic and preterminal nAChRs enhance neurotransmitter release. Postsynaptic and somal nAChRs mediate a small proportion of fast excitatory transmission and modulate cytoplasmic second messenger systems. Although the impact of nicotine obtained from tobacco is not completely understood, a portion of nicotine's addictive power is attributable to actions upon the dopaminergic systems, which normally help to reinforce rewarding behaviors. As obtained from tobacco, nicotine activates and desensitizes nAChRs, and both processes contribute to the cellular events that underlie nicotine addiction.</description><subject>Acetylcholine</subject><subject>Animals</subject><subject>Cigarettes</subject><subject>Dopamine</subject><subject>Humans</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurons - physiology</subject><subject>Nicotine - pharmacology</subject><subject>Nicotinic Agonists - pharmacology</subject><subject>Nicotinic receptor</subject><subject>Postsynaptic</subject><subject>Presynaptic</subject><subject>Receptors, Nicotinic - physiology</subject><subject>Reinforcement</subject><subject>Reward</subject><subject>Smoking</subject><subject>Substance-Related Disorders - metabolism</subject><subject>Synaptic plasticity</subject><subject>Tobacco</subject><subject>Tolerance</subject><issn>0091-3057</issn><issn>1873-5177</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMlKxEAQhhtRnHH0EZScxDlEq9JbchIZ3GDAg3pukk41tmTR7ozg25tZ0KOXqsv31_IxdopwiYDq6hmgwJSD1BeAcwAls7TYY1PMNU8lar3Ppr_IhB3F-A4AIlP6kE0QdaFQ8CmbL6hpVk0ZkpbsW9n52Makd0nnbT_4jpKyrr0dfN8dswNXNpFOdn3GXu9uXxYP6fLp_nFxs0ytEGJIlZWCc6d5AaKinFegUOVoFbjaAjgLqnB1TpSVinPNpahkjjkVqMdCjs_Y-XbuR-g_VxQH0_poxyvLjvpVNJhnUkkoRlBuQRv6GAM58xF8W4Zvg2DWjszGkVkLMIBm48isc2e7BauqpfovtZMyAtdbgMY3vzwFE62nzlLtA9nB1L3_Z8UPdeR0Xg</recordid><startdate>20011201</startdate><enddate>20011201</enddate><creator>Dani, John A.</creator><creator>De Biasi, Mariella</creator><general>Elsevier Inc</general><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>20011201</creationdate><title>Cellular mechanisms of nicotine addiction</title><author>Dani, John A. ; De Biasi, Mariella</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c444t-6c5433f73904be83b061681c60fdc00fc069fd8ee2a6337354b5818e9178e9ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Acetylcholine</topic><topic>Animals</topic><topic>Cigarettes</topic><topic>Dopamine</topic><topic>Humans</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Neurons - physiology</topic><topic>Nicotine - pharmacology</topic><topic>Nicotinic Agonists - pharmacology</topic><topic>Nicotinic receptor</topic><topic>Postsynaptic</topic><topic>Presynaptic</topic><topic>Receptors, Nicotinic - physiology</topic><topic>Reinforcement</topic><topic>Reward</topic><topic>Smoking</topic><topic>Substance-Related Disorders - metabolism</topic><topic>Synaptic plasticity</topic><topic>Tobacco</topic><topic>Tolerance</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dani, John A.</creatorcontrib><creatorcontrib>De Biasi, Mariella</creatorcontrib><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>Pharmacology, biochemistry and behavior</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dani, John A.</au><au>De Biasi, Mariella</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cellular mechanisms of nicotine addiction</atitle><jtitle>Pharmacology, biochemistry and behavior</jtitle><addtitle>Pharmacol Biochem Behav</addtitle><date>2001-12-01</date><risdate>2001</risdate><volume>70</volume><issue>4</issue><spage>439</spage><epage>446</epage><pages>439-446</pages><issn>0091-3057</issn><eissn>1873-5177</eissn><abstract>In developed countries, tobacco use is estimated to be the largest single cause of premature death [Lancet 339 (1992) 1268]. Nicotine is the main addictive component of tobacco that motivates continued use despite the harmful effects. Nicotinic acetylcholine receptors (nAChRs) are widely distributed throughout the mammalian central nervous system (CNS), where they normally respond to acetylcholine (ACh) and modulate neuronal excitability and synaptic communication. Nicotinic receptors are structurally diverse and have varied roles. Presynaptic and preterminal nAChRs enhance neurotransmitter release. Postsynaptic and somal nAChRs mediate a small proportion of fast excitatory transmission and modulate cytoplasmic second messenger systems. Although the impact of nicotine obtained from tobacco is not completely understood, a portion of nicotine's addictive power is attributable to actions upon the dopaminergic systems, which normally help to reinforce rewarding behaviors. As obtained from tobacco, nicotine activates and desensitizes nAChRs, and both processes contribute to the cellular events that underlie nicotine addiction.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>11796143</pmid><doi>10.1016/S0091-3057(01)00652-9</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0091-3057 |
| ispartof | Pharmacology, biochemistry and behavior, 2001-12, Vol.70 (4), p.439-446 |
| issn | 0091-3057 1873-5177 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_18256509 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | Acetylcholine Animals Cigarettes Dopamine Humans Neurons - drug effects Neurons - metabolism Neurons - physiology Nicotine - pharmacology Nicotinic Agonists - pharmacology Nicotinic receptor Postsynaptic Presynaptic Receptors, Nicotinic - physiology Reinforcement Reward Smoking Substance-Related Disorders - metabolism Synaptic plasticity Tobacco Tolerance |
| title | Cellular mechanisms of nicotine addiction |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-13T17%3A16%3A41IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cellular%20mechanisms%20of%20nicotine%20addiction&rft.jtitle=Pharmacology,%20biochemistry%20and%20behavior&rft.au=Dani,%20John%20A.&rft.date=2001-12-01&rft.volume=70&rft.issue=4&rft.spage=439&rft.epage=446&rft.pages=439-446&rft.issn=0091-3057&rft.eissn=1873-5177&rft_id=info:doi/10.1016/S0091-3057(01)00652-9&rft_dat=%3Cproquest_cross%3E18256509%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=18256509&rft_id=info:pmid/11796143&rft_els_id=S0091305701006529&rfr_iscdi=true |