Chronic oral nicotine treatment protects against striatal degeneration in MPTP-treated primates
Identifieur interne : 002939 ( Main/Exploration ); précédent : 002938; suivant : 002940Chronic oral nicotine treatment protects against striatal degeneration in MPTP-treated primates
Auteurs : Maryka Quik [États-Unis] ; Neeraja Parameswaran [États-Unis] ; Sarah E. Mccallum [États-Unis] ; Tanuja Bordia [États-Unis] ; SHANSHAN BAO [États-Unis] ; Alison Mccormack [États-Unis] ; Amy Kim [États-Unis] ; Rachel F. Tyndale [Canada] ; J. William Langston [États-Unis] ; Donato A. Di Monte [États-Unis]Source :
- Journal of neurochemistry [ 0022-3042 ] ; 2006.
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Abstract
The present studies were done to investigate the effect of long-term nicotine treatment against nigrostriatal damage in non-human primates. Monkeys were administered nicotine in drinking water for 6 months to provide chronic but intermittent delivery as with smoking. Plasma nicotine levels ranged from 10 to 15 ng/mL, which were within the range in cigarette smokers. Animals were then lesioned with low doses of the dopaminergic neurotoxin MPTP for several months while nicotine was continued. The results showed that levels of striatal tyrosine hydroxylase, dopamine transporter, vesicular monoamine transporter, dopamine and nicotinic receptors were greater in nicotine-treated MPTP-lesioned primates than in lesioned animals not receiving nicotine. Nicotine had no effect in unlesioned animals. Monoamine oxidase activity was similar in unlesioned and lesioned animals treated with or without nicotine, suggesting that nicotine did not exert its effects through changes in MPTP or dopamine metabolism. MPTP-induced cell loss in the substantia nigra was unaffected by nicotine treatment, indicating that nicotine acts at the striatal level to restore/maintain dopaminergic function. These data further support the possibility that nicotine contributes to the lower incidence of Parkinson's disease in smokers.
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Tyndale</name><affiliation wicri:level="4"><inist:fA14 i1="02"><s1>Center for Addiction and Mental Health and Department of Pharmacology, University of Toronto</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>8 aut.</sZ></inist:fA14><country>Canada</country><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName><orgName type="university">Université de Toronto</orgName></affiliation></author><author><name sortKey="Langston, J William" sort="Langston, J William" uniqKey="Langston J" first="J. William" last="Langston">J. William Langston</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>The Parkinson 's Institute</s1><s2>Sunnyvale, California</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Di Monte, Donato A" sort="Di Monte, Donato A" uniqKey="Di Monte D" first="Donato A." last="Di Monte">Donato A. Di Monte</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>The Parkinson 's Institute</s1><s2>Sunnyvale, California</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>7 aut.</sZ><sZ>9 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2006">2006</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Chronic</term><term>Corpus striatum</term><term>Degeneration</term><term>Human</term><term>Lesion</term><term>Long term</term><term>Monkey</term><term>Neurotoxin</term><term>Nicotine</term><term>Parkinson disease</term><term>Tobacco smoking</term><term>Treatment</term><term>Tyrosine 3-monooxygenase</term><term>Vesicular monoamine transporter</term><term>Water</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Chronique</term><term>Nicotine</term><term>Traitement</term><term>Corps strié</term><term>Dégénérescence</term><term>Long terme</term><term>Singe</term><term>Eau</term><term>Tabagisme</term><term>Animal</term><term>Lésion</term><term>Parkinson maladie</term><term>Neurotoxine</term><term>Tyrosine 3-monooxygenase</term><term>Homme</term><term>Transporteur vésiculaire monoamine</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Singe</term><term>Eau</term><term>Tabagisme</term><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The present studies were done to investigate the effect of long-term nicotine treatment against nigrostriatal damage in non-human primates. Monkeys were administered nicotine in drinking water for 6 months to provide chronic but intermittent delivery as with smoking. Plasma nicotine levels ranged from 10 to 15 ng/mL, which were within the range in cigarette smokers. Animals were then lesioned with low doses of the dopaminergic neurotoxin MPTP for several months while nicotine was continued. The results showed that levels of striatal tyrosine hydroxylase, dopamine transporter, vesicular monoamine transporter, dopamine and nicotinic receptors were greater in nicotine-treated MPTP-lesioned primates than in lesioned animals not receiving nicotine. Nicotine had no effect in unlesioned animals. Monoamine oxidase activity was similar in unlesioned and lesioned animals treated with or without nicotine, suggesting that nicotine did not exert its effects through changes in MPTP or dopamine metabolism. MPTP-induced cell loss in the substantia nigra was unaffected by nicotine treatment, indicating that nicotine acts at the striatal level to restore/maintain dopaminergic function. These data further support the possibility that nicotine contributes to the lower incidence of Parkinson's disease in smokers.</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>Californie</li><li>Ontario</li></region><settlement><li>Toronto</li></settlement><orgName><li>Université de Toronto</li></orgName></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Quik, Maryka" sort="Quik, Maryka" uniqKey="Quik M" first="Maryka" last="Quik">Maryka Quik</name></region><name sortKey="Bordia, Tanuja" sort="Bordia, Tanuja" uniqKey="Bordia T" first="Tanuja" last="Bordia">Tanuja Bordia</name><name sortKey="Di Monte, Donato A" sort="Di Monte, Donato A" uniqKey="Di Monte D" first="Donato A." last="Di Monte">Donato A. Di Monte</name><name sortKey="Kim, Amy" sort="Kim, Amy" uniqKey="Kim A" first="Amy" last="Kim">Amy Kim</name><name sortKey="Langston, J William" sort="Langston, J William" uniqKey="Langston J" first="J. William" last="Langston">J. William Langston</name><name sortKey="Mccallum, Sarah E" sort="Mccallum, Sarah E" uniqKey="Mccallum S" first="Sarah E." last="Mccallum">Sarah E. Mccallum</name><name sortKey="Mccormack, Alison" sort="Mccormack, Alison" uniqKey="Mccormack A" first="Alison" last="Mccormack">Alison Mccormack</name><name sortKey="Parameswaran, Neeraja" sort="Parameswaran, Neeraja" uniqKey="Parameswaran N" first="Neeraja" last="Parameswaran">Neeraja Parameswaran</name><name sortKey="Shanshan Bao" sort="Shanshan Bao" uniqKey="Shanshan Bao" last="Shanshan Bao">SHANSHAN BAO</name></country><country name="Canada"><region name="Ontario"><name sortKey="Tyndale, Rachel F" sort="Tyndale, Rachel F" uniqKey="Tyndale R" first="Rachel F." last="Tyndale">Rachel F. 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