Effects of bilateral striatal 6-OHDA lesions on circadian rhythms in the rat: a radiotelemetric study.
Identifieur interne : 001302 ( PubMed/Corpus ); précédent : 001301; suivant : 001303Effects of bilateral striatal 6-OHDA lesions on circadian rhythms in the rat: a radiotelemetric study.
Auteurs : V. Ben ; B. BruguerolleSource :
- Life sciences [ 0024-3205 ] ; 2000.
English descriptors
- KwdEn :
- Animals, Body Temperature (physiology), Corpus Striatum (drug effects), Disease Models, Animal, Heart Rate (physiology), Locomotion (physiology), Male, Oxidopamine, Parkinson Disease, Secondary (chemically induced), Parkinson Disease, Secondary (physiopathology), Rats, Rats, Wistar, Sleep Disorders, Circadian Rhythm (etiology), Sleep Disorders, Circadian Rhythm (physiopathology), Telemetry (methods), Weight Loss (drug effects).
- MESH :
- chemical : Oxidopamine.
- chemically induced : Parkinson Disease, Secondary.
- drug effects : Corpus Striatum, Weight Loss.
- etiology : Sleep Disorders, Circadian Rhythm.
- methods : Telemetry.
- physiology : Body Temperature, Heart Rate, Locomotion.
- physiopathology : Parkinson Disease, Secondary, Sleep Disorders, Circadian Rhythm.
- Animals, Disease Models, Animal, Male, Rats, Rats, Wistar.
Abstract
The present work aims to document, in a previously described animal model of Parkinson (double bilateral striatal injection of 6-OHDA), the possible modifications of circadian markers rhythms i.e. temperature (T), heart rate (H) and locomotor activity (A) registered continuously by telemetry, in order to evaluate a possible perturbation of the circadian rythmicity. H, T and A were measured by radiotelemetry after surgical implantation of the transmitters (Data Sciences). After a recovery period, the study was divided into a control period (C) for baseline measurements of T, H and A daily rhythms. Then, the stereotaxic 6-OHDA striatal lesion was done to a group of 4 rats while the control rats were injected into striata with saline; a second period of four registration weeks was observed [D 1-7 (W1), D 8-14 (W2), D 15-21 (W3), D 22-28 (W4)]. Finally, at the end of this period the seven rats were decapited in order to determine their striatal dopamine (DA) content. Our data document that the circadian rhythms of H, T and A were differently affected according to time. Thus, a temporary loss of circadian periodicity was observed particularly for heart rate. 6-OHDA-induced modifications of H, T and A circadian rhythm characteristics were also observed: a significant decrease of the mesor was observed for the three rhythms as well as a phase advance. Concerning the amplitude of these rhythms, only H was significantly decreased. These perturbations were observed during the four weeks following the intervention, never reaching the initial control levels. Such observed perturbations would supply a basis for the future study of the chronopharmacology of antiparkinsonian drugs.
PubMed: 10983850
Links to Exploration step
pubmed:10983850Le document en format XML
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Bruguerolle</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000</date><idno type="RBID">pubmed:10983850</idno><idno type="pmid">10983850</idno><idno type="wicri:Area/PubMed/Corpus">001302</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001302</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effects of bilateral striatal 6-OHDA lesions on circadian rhythms in the rat: a radiotelemetric study.</title><author><name sortKey="Ben, V" sort="Ben, V" uniqKey="Ben V" first="V" last="Ben">V. Ben</name><affiliation><nlm:affiliation>Laboratoire de Pharmacologie Médicale, Faculté de Médecine de Marseille, France.</nlm:affiliation></affiliation></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">Life sciences</title><idno type="ISSN">0024-3205</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Body Temperature (physiology)</term><term>Corpus Striatum (drug effects)</term><term>Disease Models, Animal</term><term>Heart Rate (physiology)</term><term>Locomotion (physiology)</term><term>Male</term><term>Oxidopamine</term><term>Parkinson Disease, Secondary (chemically induced)</term><term>Parkinson Disease, Secondary (physiopathology)</term><term>Rats</term><term>Rats, Wistar</term><term>Sleep Disorders, Circadian Rhythm (etiology)</term><term>Sleep Disorders, Circadian Rhythm (physiopathology)</term><term>Telemetry (methods)</term><term>Weight Loss (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Oxidopamine</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>Weight Loss</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Sleep Disorders, Circadian Rhythm</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Telemetry</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Body Temperature</term><term>Heart Rate</term><term>Locomotion</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease, Secondary</term><term>Sleep Disorders, Circadian Rhythm</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Male</term><term>Rats</term><term>Rats, Wistar</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The present work aims to document, in a previously described animal model of Parkinson (double bilateral striatal injection of 6-OHDA), the possible modifications of circadian markers rhythms i.e. temperature (T), heart rate (H) and locomotor activity (A) registered continuously by telemetry, in order to evaluate a possible perturbation of the circadian rythmicity. H, T and A were measured by radiotelemetry after surgical implantation of the transmitters (Data Sciences). After a recovery period, the study was divided into a control period (C) for baseline measurements of T, H and A daily rhythms. Then, the stereotaxic 6-OHDA striatal lesion was done to a group of 4 rats while the control rats were injected into striata with saline; a second period of four registration weeks was observed [D 1-7 (W1), D 8-14 (W2), D 15-21 (W3), D 22-28 (W4)]. Finally, at the end of this period the seven rats were decapited in order to determine their striatal dopamine (DA) content. Our data document that the circadian rhythms of H, T and A were differently affected according to time. Thus, a temporary loss of circadian periodicity was observed particularly for heart rate. 6-OHDA-induced modifications of H, T and A circadian rhythm characteristics were also observed: a significant decrease of the mesor was observed for the three rhythms as well as a phase advance. Concerning the amplitude of these rhythms, only H was significantly decreased. These perturbations were observed during the four weeks following the intervention, never reaching the initial control levels. Such observed perturbations would supply a basis for the future study of the chronopharmacology of antiparkinsonian drugs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10983850</PMID><DateCreated><Year>2000</Year><Month>09</Month><Day>22</Day></DateCreated><DateCompleted><Year>2000</Year><Month>09</Month><Day>22</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0024-3205</ISSN><JournalIssue CitedMedium="Print"><Volume>67</Volume><Issue>13</Issue><PubDate><Year>2000</Year><Month>Aug</Month><Day>18</Day></PubDate></JournalIssue><Title>Life sciences</Title><ISOAbbreviation>Life Sci.</ISOAbbreviation></Journal><ArticleTitle>Effects of bilateral striatal 6-OHDA lesions on circadian rhythms in the rat: a radiotelemetric study.</ArticleTitle><Pagination><MedlinePgn>1549-58</MedlinePgn></Pagination><Abstract><AbstractText>The present work aims to document, in a previously described animal model of Parkinson (double bilateral striatal injection of 6-OHDA), the possible modifications of circadian markers rhythms i.e. temperature (T), heart rate (H) and locomotor activity (A) registered continuously by telemetry, in order to evaluate a possible perturbation of the circadian rythmicity. H, T and A were measured by radiotelemetry after surgical implantation of the transmitters (Data Sciences). After a recovery period, the study was divided into a control period (C) for baseline measurements of T, H and A daily rhythms. Then, the stereotaxic 6-OHDA striatal lesion was done to a group of 4 rats while the control rats were injected into striata with saline; a second period of four registration weeks was observed [D 1-7 (W1), D 8-14 (W2), D 15-21 (W3), D 22-28 (W4)]. Finally, at the end of this period the seven rats were decapited in order to determine their striatal dopamine (DA) content. Our data document that the circadian rhythms of H, T and A were differently affected according to time. Thus, a temporary loss of circadian periodicity was observed particularly for heart rate. 6-OHDA-induced modifications of H, T and A circadian rhythm characteristics were also observed: a significant decrease of the mesor was observed for the three rhythms as well as a phase advance. Concerning the amplitude of these rhythms, only H was significantly decreased. These perturbations were observed during the four weeks following the intervention, never reaching the initial control levels. Such observed perturbations would supply a basis for the future study of the chronopharmacology of antiparkinsonian drugs.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ben</LastName><ForeName>V</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Laboratoire de Pharmacologie Médicale, Faculté de Médecine de Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bruguerolle</LastName><ForeName>B</ForeName><Initials>B</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Life Sci</MedlineTA><NlmUniqueID>0375521</NlmUniqueID><ISSNLinking>0024-3205</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>8HW4YBZ748</RegistryNumber><NameOfSubstance UI="D016627">Oxidopamine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001831" MajorTopicYN="N">Body Temperature</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003342" MajorTopicYN="N">Corpus Striatum</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006339" MajorTopicYN="N">Heart Rate</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008124" MajorTopicYN="N">Locomotion</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016627" MajorTopicYN="N">Oxidopamine</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010302" MajorTopicYN="N">Parkinson Disease, Secondary</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017208" MajorTopicYN="N">Rats, Wistar</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020178" MajorTopicYN="N">Sleep Disorders, Circadian Rhythm</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013686" MajorTopicYN="N">Telemetry</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015431" MajorTopicYN="N">Weight Loss</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2000</Year><Month>9</Month><Day>13</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2000</Year><Month>9</Month><Day>30</Day><Hour>11</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2000</Year><Month>9</Month><Day>13</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">10983850</ArticleId><ArticleId IdType="pii">S0024320500007517</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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