Endogenous nicotinic cholinergic activity regulates dopamine release in the striatum
Dopamine is vital for coordinated motion and for association learning linked to behavioral reinforcement. Here we show that the precise overlap of striatal dopaminergic and cholinergic fibers underlies potent control of dopamine release by ongoing nicotinic receptor activity. In mouse striatal slice...
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Veröffentlicht in: | Nature neuroscience 2001-12, Vol.4 (12), p.1224-1229 |
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creator | Dani, John A Zhou, Fu-Ming Liang, Yong |
description | Dopamine is vital for coordinated motion and for association learning linked to behavioral reinforcement. Here we show that the precise overlap of striatal dopaminergic and cholinergic fibers underlies potent control of dopamine release by ongoing nicotinic receptor activity. In mouse striatal slices, nicotinic antagonists or depletion of endogenous acetylcholine decreased evoked dopamine release by 90%. Nicotine at the concentration experienced by smokers also regulated dopamine release. In mutant mice lacking the β2 nicotinic subunit, evoked dopamine release was dramatically suppressed, and those mice did not show cholinergic regulation of dopamine release. The results offer new perspectives when considering nicotine addiction and the high prevalence of smoking in schizophrenics. |
doi_str_mv | 10.1038/nn769 |
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Here we show that the precise overlap of striatal dopaminergic and cholinergic fibers underlies potent control of dopamine release by ongoing nicotinic receptor activity. In mouse striatal slices, nicotinic antagonists or depletion of endogenous acetylcholine decreased evoked dopamine release by 90%. Nicotine at the concentration experienced by smokers also regulated dopamine release. In mutant mice lacking the β2 nicotinic subunit, evoked dopamine release was dramatically suppressed, and those mice did not show cholinergic regulation of dopamine release. The results offer new perspectives when considering nicotine addiction and the high prevalence of smoking in schizophrenics.</description><identifier>ISSN: 1097-6256</identifier><identifier>EISSN: 1546-1726</identifier><identifier>DOI: 10.1038/nn769</identifier><identifier>PMID: 11713470</identifier><identifier>CODEN: NANEFN</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>Acetylcholine - metabolism ; Acetylcholinesterase - metabolism ; Action Potentials - drug effects ; Action Potentials - physiology ; Animal Genetics and Genomics ; Animals ; b2 nicotinic subunit gene ; Behavioral Sciences ; Biological Techniques ; Biomedical and Life Sciences ; Biomedicine ; Calcium - metabolism ; Carbon ; Choline O-Acetyltransferase - metabolism ; Cholinergic Fibers - drug effects ; Cholinergic Fibers - metabolism ; Corpus striatum ; Dopamine ; Dopamine - metabolism ; Dopamine - secretion ; Dopaminergic mechanisms ; Enzyme Inhibitors - pharmacology ; Enzymes ; Immunohistochemistry ; Mice ; Mice, Inbred C57BL ; Muscarinic Antagonists - pharmacology ; Neostriatum - cytology ; Neostriatum - drug effects ; Neostriatum - metabolism ; Neurobiology ; Neuromuscular Depolarizing Agents - pharmacology ; Neurons - drug effects ; Neurons - metabolism ; Neurosciences ; Nicotine ; Nicotine - pharmacology ; Nicotinic Antagonists - pharmacology ; Nicotinic receptors ; Positive reinforcement ; Properties ; Publishing ; Receptors, Nicotinic - drug effects ; Receptors, Nicotinic - metabolism ; Smoking - metabolism ; Smoking - physiopathology ; Synaptic Transmission - drug effects ; Synaptic Transmission - physiology ; Tetrodotoxin - pharmacology ; Tyrosine 3-Monooxygenase - metabolism ; Voltammetry</subject><ispartof>Nature neuroscience, 2001-12, Vol.4 (12), p.1224-1229</ispartof><rights>Springer Nature America, Inc. 2001</rights><rights>COPYRIGHT 2001 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Dec 2001</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c553t-d70169a05a7214af17380c1dec84b955ecf2db41e29db829e4e71bb5041fb323</citedby><cites>FETCH-LOGICAL-c553t-d70169a05a7214af17380c1dec84b955ecf2db41e29db829e4e71bb5041fb323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/nn769$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nn769$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,2727,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11713470$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dani, John A</creatorcontrib><creatorcontrib>Zhou, Fu-Ming</creatorcontrib><creatorcontrib>Liang, Yong</creatorcontrib><title>Endogenous nicotinic cholinergic activity regulates dopamine release in the striatum</title><title>Nature neuroscience</title><addtitle>Nat Neurosci</addtitle><addtitle>Nat Neurosci</addtitle><description>Dopamine is vital for coordinated motion and for association learning linked to behavioral reinforcement. Here we show that the precise overlap of striatal dopaminergic and cholinergic fibers underlies potent control of dopamine release by ongoing nicotinic receptor activity. In mouse striatal slices, nicotinic antagonists or depletion of endogenous acetylcholine decreased evoked dopamine release by 90%. Nicotine at the concentration experienced by smokers also regulated dopamine release. In mutant mice lacking the β2 nicotinic subunit, evoked dopamine release was dramatically suppressed, and those mice did not show cholinergic regulation of dopamine release. The results offer new perspectives when considering nicotine addiction and the high prevalence of smoking in schizophrenics.</description><subject>Acetylcholine - metabolism</subject><subject>Acetylcholinesterase - metabolism</subject><subject>Action Potentials - drug effects</subject><subject>Action Potentials - physiology</subject><subject>Animal Genetics and Genomics</subject><subject>Animals</subject><subject>b2 nicotinic subunit gene</subject><subject>Behavioral Sciences</subject><subject>Biological Techniques</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Calcium - metabolism</subject><subject>Carbon</subject><subject>Choline O-Acetyltransferase - metabolism</subject><subject>Cholinergic Fibers - drug effects</subject><subject>Cholinergic Fibers - metabolism</subject><subject>Corpus striatum</subject><subject>Dopamine</subject><subject>Dopamine - metabolism</subject><subject>Dopamine - secretion</subject><subject>Dopaminergic mechanisms</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Enzymes</subject><subject>Immunohistochemistry</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Muscarinic Antagonists - pharmacology</subject><subject>Neostriatum - cytology</subject><subject>Neostriatum - drug effects</subject><subject>Neostriatum - metabolism</subject><subject>Neurobiology</subject><subject>Neuromuscular Depolarizing Agents - pharmacology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Neurosciences</subject><subject>Nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Nicotinic Antagonists - pharmacology</subject><subject>Nicotinic receptors</subject><subject>Positive reinforcement</subject><subject>Properties</subject><subject>Publishing</subject><subject>Receptors, Nicotinic - drug effects</subject><subject>Receptors, Nicotinic - metabolism</subject><subject>Smoking - metabolism</subject><subject>Smoking - physiopathology</subject><subject>Synaptic Transmission - drug effects</subject><subject>Synaptic Transmission - physiology</subject><subject>Tetrodotoxin - pharmacology</subject><subject>Tyrosine 3-Monooxygenase - metabolism</subject><subject>Voltammetry</subject><issn>1097-6256</issn><issn>1546-1726</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kV1rFTEQhoNYbK39BYIsQitebM13di9LqVooFPTch2x2dpuymxyTrNh_39Q9eGgvJJAMM88M8-ZF6ITgc4JZ88V7JdtX6IgILmuiqHxdYtyqWlIhD9HblO4xxko07Rt0SIgijCt8hDZXvg8j-LCkyjsbsit3Ze_C5DzEscTGZvfb5YcqwrhMJkOq-rA1c6mX1AQmQeV8le-gSjk6k5f5HToYzJTgZPceo83Xq83l9_rm9tv15cVNbYVgue4VJrI1WBhFCTcDUazBlvRgG961QoAdaN9xArTtu4a2wEGRrhOYk6FjlB2jT-vYbQy_FkhZzy5ZmCbjoejRjZBKtEyJQp79lyQNo5w3rIAfX4D3YYm-iNBUcUUUlrJA5ys0mgm080PI0dhyepjLF3oYXMlfkEYIKYTipeHzs4bCZPiTR7OkpK9__njOnq6sjSGlCIPeRjeb-KAJ1k9O679OF-7DbtOlm6HfUztr95pTKfkR4l7Ky0nvV9AX7yL8m7RWHwEj5Lie</recordid><startdate>20011201</startdate><enddate>20011201</enddate><creator>Dani, John A</creator><creator>Zhou, Fu-Ming</creator><creator>Liang, Yong</creator><general>Nature Publishing Group US</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>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</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>M2M</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20011201</creationdate><title>Endogenous nicotinic cholinergic activity regulates dopamine release in the striatum</title><author>Dani, John A ; Zhou, Fu-Ming ; Liang, Yong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c553t-d70169a05a7214af17380c1dec84b955ecf2db41e29db829e4e71bb5041fb323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Acetylcholine - 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Here we show that the precise overlap of striatal dopaminergic and cholinergic fibers underlies potent control of dopamine release by ongoing nicotinic receptor activity. In mouse striatal slices, nicotinic antagonists or depletion of endogenous acetylcholine decreased evoked dopamine release by 90%. Nicotine at the concentration experienced by smokers also regulated dopamine release. In mutant mice lacking the β2 nicotinic subunit, evoked dopamine release was dramatically suppressed, and those mice did not show cholinergic regulation of dopamine release. The results offer new perspectives when considering nicotine addiction and the high prevalence of smoking in schizophrenics.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><pmid>11713470</pmid><doi>10.1038/nn769</doi><tpages>6</tpages></addata></record> |
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subjects | Acetylcholine - metabolism Acetylcholinesterase - metabolism Action Potentials - drug effects Action Potentials - physiology Animal Genetics and Genomics Animals b2 nicotinic subunit gene Behavioral Sciences Biological Techniques Biomedical and Life Sciences Biomedicine Calcium - metabolism Carbon Choline O-Acetyltransferase - metabolism Cholinergic Fibers - drug effects Cholinergic Fibers - metabolism Corpus striatum Dopamine Dopamine - metabolism Dopamine - secretion Dopaminergic mechanisms Enzyme Inhibitors - pharmacology Enzymes Immunohistochemistry Mice Mice, Inbred C57BL Muscarinic Antagonists - pharmacology Neostriatum - cytology Neostriatum - drug effects Neostriatum - metabolism Neurobiology Neuromuscular Depolarizing Agents - pharmacology Neurons - drug effects Neurons - metabolism Neurosciences Nicotine Nicotine - pharmacology Nicotinic Antagonists - pharmacology Nicotinic receptors Positive reinforcement Properties Publishing Receptors, Nicotinic - drug effects Receptors, Nicotinic - metabolism Smoking - metabolism Smoking - physiopathology Synaptic Transmission - drug effects Synaptic Transmission - physiology Tetrodotoxin - pharmacology Tyrosine 3-Monooxygenase - metabolism Voltammetry |
title | Endogenous nicotinic cholinergic activity regulates dopamine release in the striatum |
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