Effect of adding the D1 agonist CY 208-243 to chronic bromocriptine treatment. I: Evaluation of motor parameters in relation to striatal catecholamine content and dopamine receptors.
Identifieur interne : 004A08 ( Ncbi/Checkpoint ); précédent : 004A07; suivant : 004A09Effect of adding the D1 agonist CY 208-243 to chronic bromocriptine treatment. I: Evaluation of motor parameters in relation to striatal catecholamine content and dopamine receptors.
Auteurs : B. Gomez-Mancilla [Canada] ; R. Boucher ; C. Gagnon ; T. Di Paolo ; R. Markstein ; P J BédardSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1993.
English descriptors
- KwdEn :
- 3,4-Dihydroxyphenylacetic Acid (metabolism), Animals, Antiparkinson Agents (administration & dosage), Bromocriptine (administration & dosage), Corpus Striatum (drug effects), Corpus Striatum (pathology), Dopamine (metabolism), Dose-Response Relationship, Drug, Drug Therapy, Combination, Homovanillic Acid (metabolism), Indoles (administration & dosage), Locomotion (drug effects), Macaca fascicularis, Motor Skills (drug effects), Motor Skills (physiology), Neurologic Examination, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (drug therapy), Parkinson Disease, Secondary (pathology), Phenanthridines (administration & dosage), Psychomotor Performance (drug effects), Receptors, Dopamine (drug effects), Receptors, Dopamine (ultrastructure), Receptors, Dopamine D1 (drug effects), Receptors, Dopamine D1 (ultrastructure).
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Bromocriptine, Indoles, Phenanthridines.
- chemical , drug effects : Receptors, Dopamine, Receptors, Dopamine D1.
- chemical , metabolism : 3,4-Dihydroxyphenylacetic Acid, Dopamine, Homovanillic Acid.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Corpus Striatum, Locomotion, Motor Skills, Psychomotor Performance.
- drug therapy : Parkinson Disease, Secondary.
- pathology : Corpus Striatum, Parkinson Disease, Secondary.
- physiology : Motor Skills.
- chemical , ultrastructure : Receptors, Dopamine, Receptors, Dopamine D1.
- Animals, Dose-Response Relationship, Drug, Drug Therapy, Combination, Macaca fascicularis, Neurologic Examination.
Abstract
A group of four cynomolgus monkeys previously rendered parkinsonian by the toxin 1-methyl-4-phenyl,1,2,3,6-tetrahydropyridine (MPTP) were observed in locomotion cages equipped with photocells during four periods of 7 days during which they received saline or two doses of the D1 agonist CY 208-243. The larger dose of 0.5 mg/kg produced a significant increase in locomotion in three of four animals. A second group of eight monkeys also previously rendered parkinsonian by MPTP and having received no other treatment were given a daily treatment of bromocriptine 1.66 mg/kg orally daily during 4 weeks. In four of the animals, after a week on bromocriptine alone, the D1 agonist CY 208-243 was added in increasing doses of 0.05, 0.1, and 0.5 mg/kg. The motor response as measured by locomotion, hand dexterity, and a disability score improved progressively at least in some of the animals on bromocriptine alone. The addition of CY 208-243 produced a more striking improvement of all three parameters, which appeared to be dose dependent. Biochemical analysis of the brain of these animals plus one control and one MPTP untreated monkey showed a > 90% loss of dopamine in the striatum in six of the eight treated monkeys. Both D2 and D1 dopamine receptors were increased in density by denervation, but both treatments abolished this increase for the D2 receptors while increasing the affinity of the D1 receptors.
DOI: 10.1002/mds.870080205
PubMed: 8474480
Affiliations:
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Gagnon</name></author><author><name sortKey="Di Paolo, T" sort="Di Paolo, T" uniqKey="Di Paolo T" first="T" last="Di Paolo">T. Di Paolo</name></author><author><name sortKey="Markstein, R" sort="Markstein, R" uniqKey="Markstein R" first="R" last="Markstein">R. Markstein</name></author><author><name sortKey="Bedard, P J" sort="Bedard, P J" uniqKey="Bedard P" first="P J" last="Bédard">P J Bédard</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1993">1993</date><idno type="RBID">pubmed:8474480</idno><idno type="pmid">8474480</idno><idno type="doi">10.1002/mds.870080205</idno><idno type="wicri:Area/PubMed/Corpus">004C58</idno><idno type="wicri:Area/PubMed/Curation">004C58</idno><idno type="wicri:Area/PubMed/Checkpoint">004C61</idno><idno type="wicri:Area/Ncbi/Merge">004A08</idno><idno type="wicri:Area/Ncbi/Curation">004A08</idno><idno type="wicri:Area/Ncbi/Checkpoint">004A08</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effect of adding the D1 agonist CY 208-243 to chronic bromocriptine treatment. I: Evaluation of motor parameters in relation to striatal catecholamine content and dopamine receptors.</title><author><name sortKey="Gomez Mancilla, B" sort="Gomez Mancilla, B" uniqKey="Gomez Mancilla B" first="B" last="Gomez-Mancilla">B. Gomez-Mancilla</name><affiliation wicri:level="1"><nlm:affiliation>School of Pharmacy, Laval University Medical Center, Sainte-Foy, Québec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>School of Pharmacy, Laval University Medical Center, Sainte-Foy, Québec</wicri:regionArea><wicri:noRegion>Québec</wicri:noRegion></affiliation></author><author><name sortKey="Boucher, R" sort="Boucher, R" uniqKey="Boucher R" first="R" last="Boucher">R. Boucher</name></author><author><name sortKey="Gagnon, C" sort="Gagnon, C" uniqKey="Gagnon C" first="C" last="Gagnon">C. Gagnon</name></author><author><name sortKey="Di Paolo, T" sort="Di Paolo, T" uniqKey="Di Paolo T" first="T" last="Di Paolo">T. Di Paolo</name></author><author><name sortKey="Markstein, R" sort="Markstein, R" uniqKey="Markstein R" first="R" last="Markstein">R. Markstein</name></author><author><name sortKey="Bedard, P J" sort="Bedard, P J" uniqKey="Bedard P" first="P J" last="Bédard">P J Bédard</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1993" type="published">1993</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid (metabolism)</term><term>Animals</term><term>Antiparkinson Agents (administration & dosage)</term><term>Bromocriptine (administration & dosage)</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (pathology)</term><term>Dopamine (metabolism)</term><term>Dose-Response Relationship, Drug</term><term>Drug Therapy, Combination</term><term>Homovanillic Acid (metabolism)</term><term>Indoles (administration & dosage)</term><term>Locomotion (drug effects)</term><term>Macaca fascicularis</term><term>Motor Skills (drug effects)</term><term>Motor Skills (physiology)</term><term>Neurologic Examination</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (drug therapy)</term><term>Parkinson Disease, Secondary (pathology)</term><term>Phenanthridines (administration & dosage)</term><term>Psychomotor Performance (drug effects)</term><term>Receptors, Dopamine (drug effects)</term><term>Receptors, Dopamine (ultrastructure)</term><term>Receptors, Dopamine D1 (drug effects)</term><term>Receptors, Dopamine D1 (ultrastructure)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Bromocriptine</term><term>Indoles</term><term>Phenanthridines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, Dopamine</term><term>Receptors, Dopamine D1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid</term><term>Dopamine</term><term>Homovanillic Acid</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Corpus Striatum</term><term>Locomotion</term><term>Motor Skills</term><term>Psychomotor Performance</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Motor Skills</term></keywords><keywords scheme="MESH" type="chemical" qualifier="ultrastructure" xml:lang="en"><term>Receptors, Dopamine</term><term>Receptors, Dopamine D1</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Dose-Response Relationship, Drug</term><term>Drug Therapy, Combination</term><term>Macaca fascicularis</term><term>Neurologic Examination</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A group of four cynomolgus monkeys previously rendered parkinsonian by the toxin 1-methyl-4-phenyl,1,2,3,6-tetrahydropyridine (MPTP) were observed in locomotion cages equipped with photocells during four periods of 7 days during which they received saline or two doses of the D1 agonist CY 208-243. The larger dose of 0.5 mg/kg produced a significant increase in locomotion in three of four animals. A second group of eight monkeys also previously rendered parkinsonian by MPTP and having received no other treatment were given a daily treatment of bromocriptine 1.66 mg/kg orally daily during 4 weeks. In four of the animals, after a week on bromocriptine alone, the D1 agonist CY 208-243 was added in increasing doses of 0.05, 0.1, and 0.5 mg/kg. The motor response as measured by locomotion, hand dexterity, and a disability score improved progressively at least in some of the animals on bromocriptine alone. The addition of CY 208-243 produced a more striking improvement of all three parameters, which appeared to be dose dependent. Biochemical analysis of the brain of these animals plus one control and one MPTP untreated monkey showed a > 90% loss of dopamine in the striatum in six of the eight treated monkeys. Both D2 and D1 dopamine receptors were increased in density by denervation, but both treatments abolished this increase for the D2 receptors while increasing the affinity of the D1 receptors.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Bedard, P J" sort="Bedard, P J" uniqKey="Bedard P" first="P J" last="Bédard">P J Bédard</name><name sortKey="Boucher, R" sort="Boucher, R" uniqKey="Boucher R" first="R" last="Boucher">R. Boucher</name><name sortKey="Di Paolo, T" sort="Di Paolo, T" uniqKey="Di Paolo T" first="T" last="Di Paolo">T. Di Paolo</name><name sortKey="Gagnon, C" sort="Gagnon, C" uniqKey="Gagnon C" first="C" last="Gagnon">C. Gagnon</name><name sortKey="Markstein, R" sort="Markstein, R" uniqKey="Markstein R" first="R" last="Markstein">R. Markstein</name></noCountry><country name="Canada"><noRegion><name sortKey="Gomez Mancilla, B" sort="Gomez Mancilla, B" uniqKey="Gomez Mancilla B" first="B" last="Gomez-Mancilla">B. Gomez-Mancilla</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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