Source:http://linkedlifedata.com/resource/pubmed/id/20736067
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions |
umls-concept:C0013384,
umls-concept:C0016904,
umls-concept:C0030685,
umls-concept:C0034693,
umls-concept:C0038590,
umls-concept:C0041904,
umls-concept:C0162493,
umls-concept:C0205217,
umls-concept:C0332281,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C0963864,
umls-concept:C1283071,
umls-concept:C1963578
|
pubmed:issue |
1
|
pubmed:dateCreated |
2010-11-16
|
pubmed:abstractText |
L-DOPA treatment induces abnormal involuntary movements (AIMs) in Parkinson's patients and experimental animals. We examined the relationship between the development of AIMs (dyskinesia) and changes in [(3)H]-GABA release and cAMP signaling in striatonigral terminals of rats with unilateral 6-OHDA lesions. Analysis of AIMs scores in hemiparkinsonian rats treated with L-DOPA for 20 days was fitted by the sum of two Gaussian distributions showing the presence of two populations: one with mild and the other with severe dyskinesia. cAMP signaling was evaluated in the two populations by determining changes in cAMP formation, G?(olf) and adenylyl cyclase type V/VI levels. In animals that were not treated with L-DOPA, all the parameters were significantly increased in the denervated side. In the animals that had mild dyskinesia, L-DOPA treatment normalized these parameters. In contrast, in the animals in which l-DOPA treatment induced severe dyskinesia all the parameters, except for G?(olf) levels, were significantly higher in the denervated side. Similarly, D1-stimulated [(3)H]-GABA release was not elevated in L-DOPA-treated animals with mild dyskinesia but was increased in animals with severe dyskinesia. Changes in G?(olf) and adenylyl cyclase type V/VI levels in the striatum paralleled the response in the SNr. The linkage between the changes in [(3)H]-GABA release and cAMP activity was further evaluated with the selective adenylyl cyclase V/VI antagonist NKY80. This inhibitor blocked the increases of both [(3)H]-GABA release and cAMP production. These results indicate that increased expression of adenylyl cyclase V/VI is a major determinant of increased GABAergic transmission in the substantia nigra pars reticulata of animals in which L-DOPA induces severe dyskinesia.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Levodopa,
http://linkedlifedata.com/resource/pubmed/chemical/Oxidopamine,
http://linkedlifedata.com/resource/pubmed/chemical/adenylyl cyclase 6,
http://linkedlifedata.com/resource/pubmed/chemical/adenylyl cyclase type V,
http://linkedlifedata.com/resource/pubmed/chemical/gamma-Aminobutyric Acid
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jan
|
pubmed:issn |
1095-953X
|
pubmed:author | |
pubmed:copyrightInfo |
Copyright © 2010 Elsevier Inc. All rights reserved.
|
pubmed:issnType |
Electronic
|
pubmed:volume |
41
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
51-61
|
pubmed:meshHeading |
pubmed-meshheading:20736067-Adenylate Cyclase,
pubmed-meshheading:20736067-Animals,
pubmed-meshheading:20736067-Dyskinesia, Drug-Induced,
pubmed-meshheading:20736067-Enzyme Inhibitors,
pubmed-meshheading:20736067-Levodopa,
pubmed-meshheading:20736067-Male,
pubmed-meshheading:20736067-Oxidopamine,
pubmed-meshheading:20736067-Parkinsonian Disorders,
pubmed-meshheading:20736067-Rats,
pubmed-meshheading:20736067-Rats, Wistar,
pubmed-meshheading:20736067-Severity of Illness Index,
pubmed-meshheading:20736067-Substantia Nigra,
pubmed-meshheading:20736067-Up-Regulation,
pubmed-meshheading:20736067-gamma-Aminobutyric Acid
|
pubmed:year |
2011
|
pubmed:articleTitle |
L-DOPA-induced dyskinesia in hemiparkinsonian rats is associated with up-regulation of adenylyl cyclase type V/VI and increased GABA release in the substantia nigra reticulata.
|
pubmed:affiliation |
Departamento de Fisiología, Biofísica y Neurociencias, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, D.F. México.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|