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Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine
Striatal dopamine (DA) release can be independently triggered not only by action potentials (APs) in dopaminergic axons but also APs in cholinergic interneurons (ChIs). Nicotine causes addiction by modulating DA release, but with paradoxical findings. Here, we investigate how physiologically relevan...
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Published in: | Nature communications 2014-05, Vol.5 (1), p.3925-3925, Article 3925 |
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creator | Wang, Li Shang, Shujiang Kang, Xinjiang Teng, Sasa Zhu, Feipeng Liu, Bin Wu, Qihui Li, Mingli Liu, Wei Xu, Huadong Zhou, Li Jiao, Ruiying Dou, Haiqiang Zuo, Panli Zhang, Xiaoyu Zheng, Lianghong Wang, Shirong Wang, Changhe Zhou, Zhuan |
description | Striatal dopamine (DA) release can be independently triggered not only by action potentials (APs) in dopaminergic axons but also APs in cholinergic interneurons (ChIs). Nicotine causes addiction by modulating DA release, but with paradoxical findings. Here, we investigate how physiologically relevant levels of nicotine modulate striatal DA release. The optogenetic stimulation of ChIs elicits DA release, which is potently inhibited by nicotine with an IC
50
of 28 nM in the dorsal striatum slice. This ChI-driven DA release is predominantly mediated by α6β2* nAChRs. Local electrical stimulus (Estim) activates both dopaminergic axons and ChIs. Nicotine does not affect the AP
DA
-dependent DA release (AP
DA
, AP of dopaminergic axon). During burst Estim, nicotine permits the facilitation of DA release by prevention of DA depletion. Our work indicates that cholinergic stimulation-induced DA release is profoundly modulated by physiologically relevant levels of nicotine and resolves the paradoxical observation of nicotine’s effects on striatal DA release.
Nicotine exposure from cigarette smoke modulates dopamine release in the brain, which is implicated in nicotine addiction, but how it does this is unclear. Here, in mouse brain slices, the authors show that nicotine inhibits cholinergic- but not dopaminergic-dependent dopamine release. |
doi_str_mv | 10.1038/ncomms4925 |
format | article |
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50
of 28 nM in the dorsal striatum slice. This ChI-driven DA release is predominantly mediated by α6β2* nAChRs. Local electrical stimulus (Estim) activates both dopaminergic axons and ChIs. Nicotine does not affect the AP
DA
-dependent DA release (AP
DA
, AP of dopaminergic axon). During burst Estim, nicotine permits the facilitation of DA release by prevention of DA depletion. Our work indicates that cholinergic stimulation-induced DA release is profoundly modulated by physiologically relevant levels of nicotine and resolves the paradoxical observation of nicotine’s effects on striatal DA release.
Nicotine exposure from cigarette smoke modulates dopamine release in the brain, which is implicated in nicotine addiction, but how it does this is unclear. Here, in mouse brain slices, the authors show that nicotine inhibits cholinergic- but not dopaminergic-dependent dopamine release.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/ncomms4925</identifier><identifier>PMID: 24968237</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13/51 ; 631/378/1689/5 ; 631/378/548/1964 ; 631/443/376 ; 64/110 ; 9/74 ; Animals ; Corpus Striatum - metabolism ; Corpus Striatum - physiology ; Dopamine - metabolism ; Electric Stimulation ; Humanities and Social Sciences ; In Vitro Techniques ; Mice ; Mice, Transgenic ; multidisciplinary ; Nicotine - metabolism ; Science ; Science (multidisciplinary)</subject><ispartof>Nature communications, 2014-05, Vol.5 (1), p.3925-3925, Article 3925</ispartof><rights>Springer Nature Limited 2014</rights><rights>Copyright Nature Publishing Group May 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c387t-a50bf66c7047f2517a919bd8e2a9b7456c86ca2de8b6cb77ddd90856fbf45a083</citedby><cites>FETCH-LOGICAL-c387t-a50bf66c7047f2517a919bd8e2a9b7456c86ca2de8b6cb77ddd90856fbf45a083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1526207804/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1526207804?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,25753,27924,27925,37012,37013,44590,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24968237$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Li</creatorcontrib><creatorcontrib>Shang, Shujiang</creatorcontrib><creatorcontrib>Kang, Xinjiang</creatorcontrib><creatorcontrib>Teng, Sasa</creatorcontrib><creatorcontrib>Zhu, Feipeng</creatorcontrib><creatorcontrib>Liu, Bin</creatorcontrib><creatorcontrib>Wu, Qihui</creatorcontrib><creatorcontrib>Li, Mingli</creatorcontrib><creatorcontrib>Liu, Wei</creatorcontrib><creatorcontrib>Xu, Huadong</creatorcontrib><creatorcontrib>Zhou, Li</creatorcontrib><creatorcontrib>Jiao, Ruiying</creatorcontrib><creatorcontrib>Dou, Haiqiang</creatorcontrib><creatorcontrib>Zuo, Panli</creatorcontrib><creatorcontrib>Zhang, Xiaoyu</creatorcontrib><creatorcontrib>Zheng, Lianghong</creatorcontrib><creatorcontrib>Wang, Shirong</creatorcontrib><creatorcontrib>Wang, Changhe</creatorcontrib><creatorcontrib>Zhou, Zhuan</creatorcontrib><title>Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><addtitle>Nat Commun</addtitle><description>Striatal dopamine (DA) release can be independently triggered not only by action potentials (APs) in dopaminergic axons but also APs in cholinergic interneurons (ChIs). Nicotine causes addiction by modulating DA release, but with paradoxical findings. Here, we investigate how physiologically relevant levels of nicotine modulate striatal DA release. The optogenetic stimulation of ChIs elicits DA release, which is potently inhibited by nicotine with an IC
50
of 28 nM in the dorsal striatum slice. This ChI-driven DA release is predominantly mediated by α6β2* nAChRs. Local electrical stimulus (Estim) activates both dopaminergic axons and ChIs. Nicotine does not affect the AP
DA
-dependent DA release (AP
DA
, AP of dopaminergic axon). During burst Estim, nicotine permits the facilitation of DA release by prevention of DA depletion. Our work indicates that cholinergic stimulation-induced DA release is profoundly modulated by physiologically relevant levels of nicotine and resolves the paradoxical observation of nicotine’s effects on striatal DA release.
Nicotine exposure from cigarette smoke modulates dopamine release in the brain, which is implicated in nicotine addiction, but how it does this is unclear. Here, in mouse brain slices, the authors show that nicotine inhibits cholinergic- but not dopaminergic-dependent dopamine release.</description><subject>13/51</subject><subject>631/378/1689/5</subject><subject>631/378/548/1964</subject><subject>631/443/376</subject><subject>64/110</subject><subject>9/74</subject><subject>Animals</subject><subject>Corpus Striatum - metabolism</subject><subject>Corpus Striatum - physiology</subject><subject>Dopamine - metabolism</subject><subject>Electric Stimulation</subject><subject>Humanities and Social Sciences</subject><subject>In Vitro Techniques</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>multidisciplinary</subject><subject>Nicotine - metabolism</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><issn>2041-1723</issn><issn>2041-1723</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNpl0E1LwzAYB_AgipO5ix9AAl5EmeatTXqU4RtMvOhRSpqmW0aazKQV9u3N3NShuTyB_Pjn4Q_ACUZXGFFx7ZRv28gKku2BI4IYHmNO6P7OfQBGMS5QOrTAgrFDMCCsyAWh_Ai8Pfm6t7Iz3kHfwNovZWuchkFbLaOGxsFurmHsgpFd38JqBZfzVTTe-plR0trVF_2QroNpaBvXMc4o36WYY3DQSBv1aDuH4PXu9mXyMJ4-3z9ObqZjRQXvxjJDVZPniiPGG5JhLgtcVLXQRBYVZ1muRK4kqbWoclVxXtd1gUSWN1XDMokEHYLzTe4y-Pdex65sTVTaWum072OJM4Ypp5RmiZ79oQvfB5e2S4rkBHGBWFIXG6WCjzHoplwG08qwKjEq172Xv70nfLqN7KtW1z_0u-UELjcgpic302Hnz_9xn7m6jlQ</recordid><startdate>20140521</startdate><enddate>20140521</enddate><creator>Wang, Li</creator><creator>Shang, Shujiang</creator><creator>Kang, Xinjiang</creator><creator>Teng, Sasa</creator><creator>Zhu, Feipeng</creator><creator>Liu, Bin</creator><creator>Wu, Qihui</creator><creator>Li, Mingli</creator><creator>Liu, Wei</creator><creator>Xu, Huadong</creator><creator>Zhou, Li</creator><creator>Jiao, Ruiying</creator><creator>Dou, Haiqiang</creator><creator>Zuo, Panli</creator><creator>Zhang, Xiaoyu</creator><creator>Zheng, Lianghong</creator><creator>Wang, Shirong</creator><creator>Wang, Changhe</creator><creator>Zhou, Zhuan</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7ST</scope><scope>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>RC3</scope><scope>SOI</scope><scope>7X8</scope></search><sort><creationdate>20140521</creationdate><title>Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine</title><author>Wang, Li ; Shang, Shujiang ; Kang, Xinjiang ; Teng, Sasa ; Zhu, Feipeng ; Liu, Bin ; Wu, Qihui ; Li, Mingli ; Liu, Wei ; Xu, Huadong ; Zhou, Li ; Jiao, Ruiying ; Dou, Haiqiang ; Zuo, Panli ; Zhang, Xiaoyu ; Zheng, Lianghong ; Wang, Shirong ; Wang, Changhe ; Zhou, Zhuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c387t-a50bf66c7047f2517a919bd8e2a9b7456c86ca2de8b6cb77ddd90856fbf45a083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>13/51</topic><topic>631/378/1689/5</topic><topic>631/378/548/1964</topic><topic>631/443/376</topic><topic>64/110</topic><topic>9/74</topic><topic>Animals</topic><topic>Corpus Striatum - 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Academic</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Li</au><au>Shang, Shujiang</au><au>Kang, Xinjiang</au><au>Teng, Sasa</au><au>Zhu, Feipeng</au><au>Liu, Bin</au><au>Wu, Qihui</au><au>Li, Mingli</au><au>Liu, Wei</au><au>Xu, Huadong</au><au>Zhou, Li</au><au>Jiao, Ruiying</au><au>Dou, Haiqiang</au><au>Zuo, Panli</au><au>Zhang, Xiaoyu</au><au>Zheng, Lianghong</au><au>Wang, Shirong</au><au>Wang, Changhe</au><au>Zhou, Zhuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><addtitle>Nat Commun</addtitle><date>2014-05-21</date><risdate>2014</risdate><volume>5</volume><issue>1</issue><spage>3925</spage><epage>3925</epage><pages>3925-3925</pages><artnum>3925</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>Striatal dopamine (DA) release can be independently triggered not only by action potentials (APs) in dopaminergic axons but also APs in cholinergic interneurons (ChIs). Nicotine causes addiction by modulating DA release, but with paradoxical findings. Here, we investigate how physiologically relevant levels of nicotine modulate striatal DA release. The optogenetic stimulation of ChIs elicits DA release, which is potently inhibited by nicotine with an IC
50
of 28 nM in the dorsal striatum slice. This ChI-driven DA release is predominantly mediated by α6β2* nAChRs. Local electrical stimulus (Estim) activates both dopaminergic axons and ChIs. Nicotine does not affect the AP
DA
-dependent DA release (AP
DA
, AP of dopaminergic axon). During burst Estim, nicotine permits the facilitation of DA release by prevention of DA depletion. Our work indicates that cholinergic stimulation-induced DA release is profoundly modulated by physiologically relevant levels of nicotine and resolves the paradoxical observation of nicotine’s effects on striatal DA release.
Nicotine exposure from cigarette smoke modulates dopamine release in the brain, which is implicated in nicotine addiction, but how it does this is unclear. Here, in mouse brain slices, the authors show that nicotine inhibits cholinergic- but not dopaminergic-dependent dopamine release.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24968237</pmid><doi>10.1038/ncomms4925</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 13/51 631/378/1689/5 631/378/548/1964 631/443/376 64/110 9/74 Animals Corpus Striatum - metabolism Corpus Striatum - physiology Dopamine - metabolism Electric Stimulation Humanities and Social Sciences In Vitro Techniques Mice Mice, Transgenic multidisciplinary Nicotine - metabolism Science Science (multidisciplinary) |
title | Modulation of dopamine release in the striatum by physiologically relevant levels of nicotine |
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