Time-dependent striatal dopamine depletion after injection of 6-hydroxydopamine in the rat. Comparison of single bilateral and double bilateral lesions.
Identifieur interne : 000088 ( Ncbi/Merge ); précédent : 000087; suivant : 000089Time-dependent striatal dopamine depletion after injection of 6-hydroxydopamine in the rat. Comparison of single bilateral and double bilateral lesions.
Auteurs : V. Ben [France] ; O. Blin ; B. BruguerolleSource :
- The Journal of pharmacy and pharmacology [ 0022-3573 ] ; 1999.
English descriptors
- KwdEn :
- 3,4-Dihydroxyphenylacetic Acid (metabolism), Animals, Chromatography, High Pressure Liquid, Corpus Striatum (drug effects), Corpus Striatum (metabolism), Disease Models, Animal, Dopamine (metabolism), Functional Laterality, Injections, Male, Oxidopamine (administration & dosage), Oxidopamine (toxicity), Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (metabolism), Parkinson Disease, Secondary (physiopathology), Rats, Rats, Wistar.
- MESH :
- chemical , administration & dosage : Oxidopamine.
- chemical , metabolism : 3,4-Dihydroxyphenylacetic Acid, Dopamine.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Corpus Striatum.
- metabolism : Corpus Striatum, Parkinson Disease, Secondary.
- physiopathology : Parkinson Disease, Secondary.
- chemical , toxicity : Oxidopamine.
- Animals, Chromatography, High Pressure Liquid, Disease Models, Animal, Functional Laterality, Injections, Male, Rats, Rats, Wistar.
Abstract
For future investigation of possible perturbation of circadian rhythm in animal models of Parkinson's disease we needed an animal model providing lasting 80-100% striatal dopaminergic depletion in rats, but without induced mortality. We have thus compared the effects of a single hydroxydopamine bilateral striatal lesion (SB-hydroxydopamine) with those of a double hydroxydopamine bilateral lesion (DB-hydroxydopamine) at the same dose (16 microg/striatum) by HPLC determination of dopamine and 3,4-dihydrophenylacetic acid (dopac) levels in the striatum. Two weeks after neurosurgery, SB-hydroxydopamine and DB-hydroxydopamine induced dopaminergic depletion of at least 81% compared with control groups. After eight weeks striatal dopaminergic depletion was only 60.97% in SB-hydroxydopamine rats, suggesting a compensatory phenomenon, whereas in DB-hydroxydopamine rats dopaminergic loss was stable at 88%. For the DB-hydroxydopamine group the dopac/dopamine ratio was significantly increased at week 2 only, whereas no significant change was observed for other groups. This increase might be explained by increased dopamine turnover. We have demonstrated that striatal DB-hydroxydopamine injection induces lasting 80-100% neuronal loss, close to that observed in the disease in man, without induced mortality, and provides a tool which meets our experimental requirements.
PubMed: 10678495
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Blin</name></author><author><name sortKey="Bruguerolle, B" sort="Bruguerolle, B" uniqKey="Bruguerolle B" first="B" last="Bruguerolle">B. Bruguerolle</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1999">1999</date><idno type="RBID">pubmed:10678495</idno><idno type="pmid">10678495</idno><idno type="wicri:Area/PubMed/Corpus">001360</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001360</idno><idno type="wicri:Area/PubMed/Curation">001319</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001319</idno><idno type="wicri:Area/PubMed/Checkpoint">001319</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001319</idno><idno type="wicri:Area/Ncbi/Merge">000088</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Time-dependent striatal dopamine depletion after injection of 6-hydroxydopamine in the rat. Comparison of single bilateral and double bilateral lesions.</title><author><name sortKey="Ben, V" sort="Ben, V" uniqKey="Ben V" first="V" last="Ben">V. Ben</name><affiliation wicri:level="3"><nlm:affiliation>Department of Medical and Clinical Pharmacology, Faculty of Medicine, Marseille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Department of Medical and Clinical Pharmacology, Faculty of Medicine, Marseille</wicri:regionArea><placeName><region type="region">Provence-Alpes-Côte d'Azur</region><region type="old region">Provence-Alpes-Côte d'Azur</region><settlement type="city">Marseille</settlement></placeName></affiliation></author><author><name sortKey="Blin, O" sort="Blin, O" uniqKey="Blin O" first="O" last="Blin">O. Blin</name></author><author><name sortKey="Bruguerolle, B" sort="Bruguerolle, B" uniqKey="Bruguerolle B" first="B" last="Bruguerolle">B. Bruguerolle</name></author></analytic><series><title level="j">The Journal of pharmacy and pharmacology</title><idno type="ISSN">0022-3573</idno><imprint><date when="1999" type="published">1999</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>Chromatography, High Pressure Liquid</term><term>Corpus Striatum (drug effects)</term><term>Corpus Striatum (metabolism)</term><term>Disease Models, Animal</term><term>Dopamine (metabolism)</term><term>Functional Laterality</term><term>Injections</term><term>Male</term><term>Oxidopamine (administration & dosage)</term><term>Oxidopamine (toxicity)</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (metabolism)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Rats</term><term>Rats, Wistar</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Oxidopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>3,4-Dihydroxyphenylacetic Acid</term><term>Dopamine</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></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Corpus Striatum</term><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease, Secondary</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Oxidopamine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Chromatography, High Pressure Liquid</term><term>Disease Models, Animal</term><term>Functional Laterality</term><term>Injections</term><term>Male</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">For future investigation of possible perturbation of circadian rhythm in animal models of Parkinson's disease we needed an animal model providing lasting 80-100% striatal dopaminergic depletion in rats, but without induced mortality. We have thus compared the effects of a single hydroxydopamine bilateral striatal lesion (SB-hydroxydopamine) with those of a double hydroxydopamine bilateral lesion (DB-hydroxydopamine) at the same dose (16 microg/striatum) by HPLC determination of dopamine and 3,4-dihydrophenylacetic acid (dopac) levels in the striatum. Two weeks after neurosurgery, SB-hydroxydopamine and DB-hydroxydopamine induced dopaminergic depletion of at least 81% compared with control groups. After eight weeks striatal dopaminergic depletion was only 60.97% in SB-hydroxydopamine rats, suggesting a compensatory phenomenon, whereas in DB-hydroxydopamine rats dopaminergic loss was stable at 88%. For the DB-hydroxydopamine group the dopac/dopamine ratio was significantly increased at week 2 only, whereas no significant change was observed for other groups. This increase might be explained by increased dopamine turnover. We have demonstrated that striatal DB-hydroxydopamine injection induces lasting 80-100% neuronal loss, close to that observed in the disease in man, without induced mortality, and provides a tool which meets our experimental requirements.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10678495</PMID><DateCreated><Year>2000</Year><Month>03</Month><Day>02</Day></DateCreated><DateCompleted><Year>2000</Year><Month>03</Month><Day>02</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-3573</ISSN><JournalIssue CitedMedium="Print"><Volume>51</Volume><Issue>12</Issue><PubDate><Year>1999</Year><Month>Dec</Month></PubDate></JournalIssue><Title>The Journal of pharmacy and pharmacology</Title><ISOAbbreviation>J. Pharm. Pharmacol.</ISOAbbreviation></Journal><ArticleTitle>Time-dependent striatal dopamine depletion after injection of 6-hydroxydopamine in the rat. Comparison of single bilateral and double bilateral lesions.</ArticleTitle><Pagination><MedlinePgn>1405-8</MedlinePgn></Pagination><Abstract><AbstractText>For future investigation of possible perturbation of circadian rhythm in animal models of Parkinson's disease we needed an animal model providing lasting 80-100% striatal dopaminergic depletion in rats, but without induced mortality. We have thus compared the effects of a single hydroxydopamine bilateral striatal lesion (SB-hydroxydopamine) with those of a double hydroxydopamine bilateral lesion (DB-hydroxydopamine) at the same dose (16 microg/striatum) by HPLC determination of dopamine and 3,4-dihydrophenylacetic acid (dopac) levels in the striatum. Two weeks after neurosurgery, SB-hydroxydopamine and DB-hydroxydopamine induced dopaminergic depletion of at least 81% compared with control groups. After eight weeks striatal dopaminergic depletion was only 60.97% in SB-hydroxydopamine rats, suggesting a compensatory phenomenon, whereas in DB-hydroxydopamine rats dopaminergic loss was stable at 88%. For the DB-hydroxydopamine group the dopac/dopamine ratio was significantly increased at week 2 only, whereas no significant change was observed for other groups. This increase might be explained by increased dopamine turnover. 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Blin</name><name sortKey="Bruguerolle, B" sort="Bruguerolle, B" uniqKey="Bruguerolle B" first="B" last="Bruguerolle">B. Bruguerolle</name></noCountry><country name="France"><region name="Provence-Alpes-Côte d'Azur"><name sortKey="Ben, V" sort="Ben, V" uniqKey="Ben V" first="V" last="Ben">V. Ben</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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