Linked Life Data

14552886

Source:http://linkedlifedata.com/resource/pubmed/id/14552886

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-10-13
pubmed:abstractText
Long-term treatment of Parkinson's disease with levodopa is compromised by the development of motor complications, including on-off fluctuations and involuntary movements termed dyskinesia. The neural mechanisms underlying treatment-related dyskinesias may involve underactivity of the output regions of the basal ganglia, i.e., the medial segment of the globus pallidus (GPm) and substantia nigra pars reticulata (SNR). Increased activity of GABAergic neurons of the "direct" striatopallidal pathway has been implicated in the suppression of the GPm and SNR and thus the development of dyskinesia. The direct pathway uses opioids as a co-neurotransmitter. These opioid peptides are products of the high-molecular weight opioid precursor pre-proenkephalin B (PPE-B). In situ hybridisation studies were employed to investigate PPE-B mRNA expression in postmortem striatal tissue from patients with a clinicopathological diagnosis of Parkinson's disease, all of whom displayed levodopa-induced motor complications, including dyskinesia prior to death and in the caudate-putamen (striatum) of the MPTP-lesioned macaque model of Parkinson's disease with treatment-related dyskinesia. Striatal PPE-B mRNA expression was significantly increased by 172% in dyskinetic Parkinson's disease patients compared to age-matched controls. This increase was heterogeneous with increased expression within the striosomes compared to matrix compartments of the striatum. Striatal PPE-B mRNA expression was significantly increased by 185% in the MPTP-lesioned macaque exhibiting dyskinesia, compared to parkinsonian, nondyskinetic MPTP-lesioned macaques, and by 146% compared to non-parkinsonian, nondyskinetic controls. Increased PPE-B mRNA expression, with subsequent elevations in opioid peptide transmission within the direct striatal output pathways, may underlie treatment-related dyskinesia in Parkinson's disease.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0014-4886
pubmed:author
pubmed:issnType
Print
pubmed:volume
183
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
458-68
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Increased striatal pre-proenkephalin B expression is associated with dyskinesia in Parkinson's disease.
pubmed:affiliation
Manchester Movement Disorder Laboratory, 1.124 Division of Neuroscience, School of Biological Sciences, Stopford Building, University of Manchester, Oxford Road, M13 9PT, Manchester, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't