Dopamine D1 receptor mRNA and receptor levels in the striatum of MPTP monkeys chronically treated with SKF-82958
Identifieur interne : 000D50 ( PascalFrancis/Corpus ); précédent : 000D49; suivant : 000D51Dopamine D1 receptor mRNA and receptor levels in the striatum of MPTP monkeys chronically treated with SKF-82958
Auteurs : R. Grondin ; M. Goulet ; M. Morissette ; P. J. Bedard ; T. Di PaoloSource :
- European journal of pharmacology [ 0014-2999 ] ; 1999.
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Abstract
The density of dopamine D1 receptor antagonist sites was measured by autoradiography and dopamine D1 receptor mRNA levels were measured by in situ hybridization in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-exposed monkeys chronically treated with the dopamine D1 receptor agonist 6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrobromide (SKF-82958) administered in intermittent or continuous mode for a month. Normal and MPTP-exposed but otherwise untreated animals were used for comparison. Intermittent treatment with SKF-82958 relieved parkinsonian features and induced dyskinesias whereas given continuously this drug induced behavioral tolerance without dyskinesias. On the one hand, MPTP treatment tended to increase dopamine D1receptor density in the putamen whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant increase compared to control animals. On the other hand, dopamine D1 receptor mRNA levels in the putamen appeared to decrease after MPTP lesion and agonist treatment as compared to dopamine D1receptor density. In contrast, an apparent decrease in dopamine D1 receptor density and mRNA levels was observed in the nucleus accumbens of untreated MPTP monkeys whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant decrease compared to control animals. Thus, neither dyskinesias nor tolerance can be exclusively related to an increase or decrease in striatal dopamine D, receptors, respectively.
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| NO : | PASCAL 99-0436170 INIST |
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| ET : | Dopamine D1 receptor mRNA and receptor levels in the striatum of MPTP monkeys chronically treated with SKF-82958 |
| AU : | GRONDIN (R.); GOULET (M.); MORISSETTE (M.); BEDARD (P. J.); DI PAOLO (T.) |
| AF : | Faculty of Medicine, Laval University/Quebec City, G1K 7P4/Canada (1 aut., 4 aut.); Molecular Endocrinology Research Unit, Laval University Research Center, 2705 Laurier Blvd/Quebec City, G1V 4G2/Canada (1 aut., 2 aut., 3 aut., 5 aut.); Neuroscience Research Unit, Laval University Research Center, 2705 Laurier Blvd/Quebec City, G1V 4G2/Canada (1 aut., 4 aut.); Faculty of Pharmacy, Laval University/Quebec City, GIK 7P4/Canada (2 aut., 5 aut.) |
| DT : | Publication en série; Courte communication, note brève; Niveau analytique |
| SO : | European journal of pharmacology; ISSN 0014-2999; Coden EJPHAZ; Pays-Bas; Da. 1999; Vol. 378; No. 3; Pp. 259-263; Bibl. 18 ref. |
| LA : | Anglais |
| EA : | The density of dopamine D1 receptor antagonist sites was measured by autoradiography and dopamine D1 receptor mRNA levels were measured by in situ hybridization in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-exposed monkeys chronically treated with the dopamine D1 receptor agonist 6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrobromide (SKF-82958) administered in intermittent or continuous mode for a month. Normal and MPTP-exposed but otherwise untreated animals were used for comparison. Intermittent treatment with SKF-82958 relieved parkinsonian features and induced dyskinesias whereas given continuously this drug induced behavioral tolerance without dyskinesias. On the one hand, MPTP treatment tended to increase dopamine D1receptor density in the putamen whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant increase compared to control animals. On the other hand, dopamine D1 receptor mRNA levels in the putamen appeared to decrease after MPTP lesion and agonist treatment as compared to dopamine D1receptor density. In contrast, an apparent decrease in dopamine D1 receptor density and mRNA levels was observed in the nucleus accumbens of untreated MPTP monkeys whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant decrease compared to control animals. Thus, neither dyskinesias nor tolerance can be exclusively related to an increase or decrease in striatal dopamine D, receptors, respectively. |
| CC : | 002B02B06 |
| FD : | Antiparkinsonien; Récepteur dopaminergique D1; Agoniste; Parkinson maladie; Dyskinésie; Corps strié; Système nerveux central; Encéphale; Putamen; Animal; Singe; Long terme; Voie souscutanée; Pompe osmotique; Forme libération lente; Dopamine; Catécholamine; Messager secondaire; SKF 82958 |
| FG : | Primates; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Trouble neurologique; Mouvement involontaire |
| ED : | Antiparkinson agent; D1 Dopamine receptor; Agonist; Parkinson disease; Dyskinesia; Corpus striatum; Central nervous system; Brain (vertebrata); Putamen; Animal; Monkey; Long term; Subcutaneous administration; Osmotic pump; Slow release form; Dopamine; Catecholamine; Second messenger |
| EG : | Primates; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Neurological disorder; Involuntary movement |
| SD : | Antiparkinsoniano; Receptor dopaminérgico D1; Agonista; Parkinson enfermedad; Disquinesia; Cuerpo estriado; Sistema nervioso central; Encéfalo; Putamen; Animal; Mono; Largo plazo; Vía subcutánea; Bomba osmótica; Forma liberación lente; Dopamina; Catecolamina; Mensajero segundo |
| LO : | INIST-13322.354000085925380030 |
| ID : | 99-0436170 |
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Grondin</name><affiliation><inist:fA14 i1="01"><s1>Faculty of Medicine, Laval University</s1><s2>Quebec City, G1K 7P4</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Molecular Endocrinology Research Unit, Laval University Research Center, 2705 Laurier Blvd</s1><s2>Quebec City, G1V 4G2</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Neuroscience Research Unit, Laval University Research Center, 2705 Laurier Blvd</s1><s2>Quebec City, G1V 4G2</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Goulet, M" sort="Goulet, M" uniqKey="Goulet M" first="M." last="Goulet">M. Goulet</name><affiliation><inist:fA14 i1="02"><s1>Molecular Endocrinology Research Unit, Laval University Research Center, 2705 Laurier Blvd</s1><s2>Quebec City, G1V 4G2</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Faculty of Pharmacy, Laval University</s1><s2>Quebec City, GIK 7P4</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Morissette, M" sort="Morissette, M" uniqKey="Morissette M" first="M." last="Morissette">M. Morissette</name><affiliation><inist:fA14 i1="02"><s1>Molecular Endocrinology Research Unit, Laval University Research Center, 2705 Laurier Blvd</s1><s2>Quebec City, G1V 4G2</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Bedard, P J" sort="Bedard, P J" uniqKey="Bedard P" first="P. J." last="Bedard">P. J. Bedard</name><affiliation><inist:fA14 i1="01"><s1>Faculty of Medicine, Laval University</s1><s2>Quebec City, G1K 7P4</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="03"><s1>Neuroscience Research Unit, Laval University Research Center, 2705 Laurier Blvd</s1><s2>Quebec City, G1V 4G2</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Di Paolo, T" sort="Di Paolo, T" uniqKey="Di Paolo T" first="T." last="Di Paolo">T. Di Paolo</name><affiliation><inist:fA14 i1="02"><s1>Molecular Endocrinology Research Unit, Laval University Research Center, 2705 Laurier Blvd</s1><s2>Quebec City, G1V 4G2</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Faculty of Pharmacy, Laval University</s1><s2>Quebec City, GIK 7P4</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">European journal of pharmacology</title><title level="j" type="abbreviated">Eur. j. pharmacol.</title><idno type="ISSN">0014-2999</idno><imprint><date when="1999">1999</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">European journal of pharmacology</title><title level="j" type="abbreviated">Eur. j. pharmacol.</title><idno type="ISSN">0014-2999</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Agonist</term><term>Animal</term><term>Antiparkinson agent</term><term>Brain (vertebrata)</term><term>Catecholamine</term><term>Central nervous system</term><term>Corpus striatum</term><term>D1 Dopamine receptor</term><term>Dopamine</term><term>Dyskinesia</term><term>Long term</term><term>Monkey</term><term>Osmotic pump</term><term>Parkinson disease</term><term>Putamen</term><term>Second messenger</term><term>Slow release form</term><term>Subcutaneous administration</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Antiparkinsonien</term><term>Récepteur dopaminergique D1</term><term>Agoniste</term><term>Parkinson maladie</term><term>Dyskinésie</term><term>Corps strié</term><term>Système nerveux central</term><term>Encéphale</term><term>Putamen</term><term>Animal</term><term>Singe</term><term>Long terme</term><term>Voie souscutanée</term><term>Pompe osmotique</term><term>Forme libération lente</term><term>Dopamine</term><term>Catécholamine</term><term>Messager secondaire</term><term>SKF 82958</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The density of dopamine D<sub>1</sub> receptor antagonist sites was measured by autoradiography and dopamine D<sub>1</sub> receptor mRNA levels were measured by in situ hybridization in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-exposed monkeys chronically treated with the dopamine D<sub>1</sub> receptor agonist 6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrobromide (SKF-82958) administered in intermittent or continuous mode for a month. Normal and MPTP-exposed but otherwise untreated animals were used for comparison. Intermittent treatment with SKF-82958 relieved parkinsonian features and induced dyskinesias whereas given continuously this drug induced behavioral tolerance without dyskinesias. On the one hand, MPTP treatment tended to increase dopamine D<sub>1</sub>receptor density in the putamen whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant increase compared to control animals. On the other hand, dopamine D<sub>1</sub> receptor mRNA levels in the putamen appeared to decrease after MPTP lesion and agonist treatment as compared to dopamine D<sub>1</sub>receptor density. In contrast, an apparent decrease in dopamine D<sub>1</sub> receptor density and mRNA levels was observed in the nucleus accumbens of untreated MPTP monkeys whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant decrease compared to control animals. Thus, neither dyskinesias nor tolerance can be exclusively related to an increase or decrease in striatal dopamine D, receptors, respectively.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0014-2999</s0></fA01><fA02 i1="01"><s0>EJPHAZ</s0></fA02><fA03 i2="1"><s0>Eur. j. pharmacol.</s0></fA03><fA05><s2>378</s2></fA05><fA06><s2>3</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Dopamine D<sub>1</sub> receptor mRNA and receptor levels in the striatum of MPTP monkeys chronically treated with SKF-82958</s1></fA08><fA11 i1="01" i2="1"><s1>GRONDIN (R.)</s1></fA11><fA11 i1="02" i2="1"><s1>GOULET (M.)</s1></fA11><fA11 i1="03" i2="1"><s1>MORISSETTE (M.)</s1></fA11><fA11 i1="04" i2="1"><s1>BEDARD (P. J.)</s1></fA11><fA11 i1="05" i2="1"><s1>DI PAOLO (T.)</s1></fA11><fA14 i1="01"><s1>Faculty of Medicine, Laval University</s1><s2>Quebec City, G1K 7P4</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="02"><s1>Molecular Endocrinology Research Unit, Laval University Research Center, 2705 Laurier Blvd</s1><s2>Quebec City, G1V 4G2</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>5 aut.</sZ></fA14><fA14 i1="03"><s1>Neuroscience Research Unit, Laval University Research Center, 2705 Laurier Blvd</s1><s2>Quebec City, G1V 4G2</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></fA14><fA14 i1="04"><s1>Faculty of Pharmacy, Laval University</s1><s2>Quebec City, GIK 7P4</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>5 aut.</sZ></fA14><fA20><s1>259-263</s1></fA20><fA21><s1>1999</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>13322</s2><s5>354000085925380030</s5></fA43><fA44><s0>0000</s0><s1>© 1999 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>18 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>99-0436170</s0></fA47><fA60><s1>P</s1><s3>CC</s3></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>European journal of pharmacology</s0></fA64><fA66 i1="01"><s0>NLD</s0></fA66><fC01 i1="01" l="ENG"><s0>The density of dopamine D<sub>1</sub> receptor antagonist sites was measured by autoradiography and dopamine D<sub>1</sub> receptor mRNA levels were measured by in situ hybridization in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-exposed monkeys chronically treated with the dopamine D<sub>1</sub> receptor agonist 6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrobromide (SKF-82958) administered in intermittent or continuous mode for a month. Normal and MPTP-exposed but otherwise untreated animals were used for comparison. Intermittent treatment with SKF-82958 relieved parkinsonian features and induced dyskinesias whereas given continuously this drug induced behavioral tolerance without dyskinesias. On the one hand, MPTP treatment tended to increase dopamine D<sub>1</sub>receptor density in the putamen whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant increase compared to control animals. On the other hand, dopamine D<sub>1</sub> receptor mRNA levels in the putamen appeared to decrease after MPTP lesion and agonist treatment as compared to dopamine D<sub>1</sub>receptor density. In contrast, an apparent decrease in dopamine D<sub>1</sub> receptor density and mRNA levels was observed in the nucleus accumbens of untreated MPTP monkeys whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant decrease compared to control animals. Thus, neither dyskinesias nor tolerance can be exclusively related to an increase or decrease in striatal dopamine D, receptors, respectively.</s0></fC01><fC02 i1="01" i2="X"><s0>002B02B06</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Antiparkinsonien</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Antiparkinson agent</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Antiparkinsoniano</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Récepteur dopaminergique D1</s0><s5>04</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>D1 Dopamine receptor</s0><s5>04</s5><s6>«D1» Dopamine receptor</s6></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Receptor dopaminérgico D1</s0><s5>04</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Agoniste</s0><s5>05</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Agonist</s0><s5>05</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Agonista</s0><s5>05</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Parkinson maladie</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Parkinson 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l="FRE"><s0>Putamen</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Putamen</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Putamen</s0><s5>15</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Animal</s0><s5>16</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Animal</s0><s5>16</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Animal</s0><s5>16</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Singe</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Monkey</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Mono</s0><s5>17</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Long terme</s0><s5>18</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Long term</s0><s5>18</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Largo plazo</s0><s5>18</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Voie souscutanée</s0><s5>19</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Subcutaneous administration</s0><s5>19</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Vía subcutánea</s0><s5>19</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Pompe osmotique</s0><s5>20</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>Osmotic pump</s0><s5>20</s5></fC03><fC03 i1="14" i2="X" l="SPA"><s0>Bomba osmótica</s0><s5>20</s5></fC03><fC03 i1="15" i2="X" l="FRE"><s0>Forme libération lente</s0><s5>21</s5></fC03><fC03 i1="15" i2="X" l="ENG"><s0>Slow release form</s0><s5>21</s5></fC03><fC03 i1="15" i2="X" l="SPA"><s0>Forma liberación lente</s0><s5>21</s5></fC03><fC03 i1="16" i2="X" l="FRE"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>22</s5></fC03><fC03 i1="16" i2="X" l="ENG"><s0>Dopamine</s0><s2>NK</s2><s2>FR</s2><s5>22</s5></fC03><fC03 i1="16" i2="X" l="SPA"><s0>Dopamina</s0><s2>NK</s2><s2>FR</s2><s5>22</s5></fC03><fC03 i1="17" i2="X" l="FRE"><s0>Catécholamine</s0><s5>23</s5></fC03><fC03 i1="17" i2="X" l="ENG"><s0>Catecholamine</s0><s5>23</s5></fC03><fC03 i1="17" i2="X" l="SPA"><s0>Catecolamina</s0><s5>23</s5></fC03><fC03 i1="18" i2="X" l="FRE"><s0>Messager secondaire</s0><s5>24</s5></fC03><fC03 i1="18" i2="X" l="ENG"><s0>Second messenger</s0><s5>24</s5></fC03><fC03 i1="18" i2="X" l="SPA"><s0>Mensajero segundo</s0><s5>24</s5></fC03><fC03 i1="19" i2="X" l="FRE"><s0>SKF 82958</s0><s2>FR</s2><s4>INC</s4><s5>86</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Primates</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Primates</s0><s2>NS</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Primates</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Vertebrata</s0><s2>NS</s2></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>53</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>53</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>53</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>54</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>54</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>54</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>55</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>55</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>55</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0><s5>56</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>56</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>56</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>57</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>57</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>57</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Trouble neurologique</s0><s5>62</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Neurological disorder</s0><s5>62</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Trastorno neurológico</s0><s5>62</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Mouvement involontaire</s0><s5>63</s5></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Involuntary movement</s0><s5>63</s5></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Movimiento involuntario</s0><s5>63</s5></fC07><fN21><s1>277</s1></fN21></pA></standard><server><NO>PASCAL 99-0436170 INIST</NO><ET>Dopamine D<sub>1</sub> receptor mRNA and receptor levels in the striatum of MPTP monkeys chronically treated with SKF-82958</ET><AU>GRONDIN (R.); GOULET (M.); MORISSETTE (M.); BEDARD (P. J.); DI PAOLO (T.)</AU><AF>Faculty of Medicine, Laval University/Quebec City, G1K 7P4/Canada (1 aut., 4 aut.); Molecular Endocrinology Research Unit, Laval University Research Center, 2705 Laurier Blvd/Quebec City, G1V 4G2/Canada (1 aut., 2 aut., 3 aut., 5 aut.); Neuroscience Research Unit, Laval University Research Center, 2705 Laurier Blvd/Quebec City, G1V 4G2/Canada (1 aut., 4 aut.); Faculty of Pharmacy, Laval University/Quebec City, GIK 7P4/Canada (2 aut., 5 aut.)</AF><DT>Publication en série; Courte communication, note brève; Niveau analytique</DT><SO>European journal of pharmacology; ISSN 0014-2999; Coden EJPHAZ; Pays-Bas; Da. 1999; Vol. 378; No. 3; Pp. 259-263; Bibl. 18 ref.</SO><LA>Anglais</LA><EA>The density of dopamine D<sub>1</sub> receptor antagonist sites was measured by autoradiography and dopamine D<sub>1</sub> receptor mRNA levels were measured by in situ hybridization in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-exposed monkeys chronically treated with the dopamine D<sub>1</sub> receptor agonist 6-chloro-7,8-dihydroxy-3-allyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrobromide (SKF-82958) administered in intermittent or continuous mode for a month. Normal and MPTP-exposed but otherwise untreated animals were used for comparison. Intermittent treatment with SKF-82958 relieved parkinsonian features and induced dyskinesias whereas given continuously this drug induced behavioral tolerance without dyskinesias. On the one hand, MPTP treatment tended to increase dopamine D<sub>1</sub>receptor density in the putamen whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant increase compared to control animals. On the other hand, dopamine D<sub>1</sub> receptor mRNA levels in the putamen appeared to decrease after MPTP lesion and agonist treatment as compared to dopamine D<sub>1</sub>receptor density. In contrast, an apparent decrease in dopamine D<sub>1</sub> receptor density and mRNA levels was observed in the nucleus accumbens of untreated MPTP monkeys whereas treatment of MPTP monkeys with SKF-82958, intermittent or continuous, produced a significant decrease compared to control animals. Thus, neither dyskinesias nor tolerance can be exclusively related to an increase or decrease in striatal dopamine D, receptors, respectively.</EA><CC>002B02B06</CC><FD>Antiparkinsonien; Récepteur dopaminergique D1; Agoniste; Parkinson maladie; Dyskinésie; Corps strié; Système nerveux central; Encéphale; Putamen; Animal; Singe; Long terme; Voie souscutanée; Pompe osmotique; Forme libération lente; Dopamine; Catécholamine; Messager secondaire; SKF 82958</FD><FG>Primates; Mammalia; Vertebrata; Système nerveux pathologie; Système nerveux central pathologie; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Trouble neurologique; Mouvement involontaire</FG><ED>Antiparkinson agent; D1 Dopamine receptor; Agonist; Parkinson disease; Dyskinesia; Corpus striatum; Central nervous system; Brain (vertebrata); Putamen; Animal; Monkey; Long term; Subcutaneous administration; Osmotic pump; Slow release form; Dopamine; Catecholamine; Second messenger</ED><EG>Primates; Mammalia; Vertebrata; Nervous system diseases; Central nervous system disease; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Neurological disorder; Involuntary movement</EG><SD>Antiparkinsoniano; Receptor dopaminérgico D1; Agonista; Parkinson enfermedad; Disquinesia; Cuerpo estriado; Sistema nervioso central; Encéfalo; Putamen; Animal; Mono; Largo plazo; Vía subcutánea; Bomba osmótica; Forma liberación lente; Dopamina; Catecolamina; Mensajero segundo</SD><LO>INIST-13322.354000085925380030</LO><ID>99-0436170</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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