Striatal expression of substance P and methionin-enkephalin in genes in patients with Parkinson's disease.
Identifieur interne : 001473 ( PubMed/Checkpoint ); précédent : 001472; suivant : 001474Striatal expression of substance P and methionin-enkephalin in genes in patients with Parkinson's disease.
Auteurs : R. Levy [France] ; M. Vila ; M T Herrero ; B. Faucheux ; Yves Agid [France] ; E C HirschSource :
- Neuroscience letters [ 0304-3940 ] ; 1995.
English descriptors
- KwdEn :
- MESH :
- chemical , genetics : Enkephalin, Methionine, Substance P.
- genetics : Parkinson Disease.
- metabolism : Caudate Nucleus, Corpus Striatum, Parkinson Disease, Putamen, RNA, Messenger, Substance P.
- Aged, Humans, In Situ Hybridization.
Abstract
The striatal expression of substance P (SP) and methionin-enkephalin (met-enk) genes was studied post mortem by in situ hybridization in patients with Parkinson's disease and a group of control subjects. No significant difference in striatal expression of these two neuropeptide messenger RNAs (mRNAs) was found in the patients compared with control subjects. This contrasts with animal models of parkinsonism, where expression of SP mRNA is decreased and met-enk mRNA increased. Possible explanations include: (1) compensatory mechanisms, which may develop during the long term evolution of Parkinson's disease; (2) normalized expression of the two genes resulting from chronic L-DOPA therapy.
PubMed: 8577402
Affiliations:
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pubmed:8577402Le document en format XML
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<front><div type="abstract" xml:lang="en">The striatal expression of substance P (SP) and methionin-enkephalin (met-enk) genes was studied post mortem by in situ hybridization in patients with Parkinson's disease and a group of control subjects. No significant difference in striatal expression of these two neuropeptide messenger RNAs (mRNAs) was found in the patients compared with control subjects. This contrasts with animal models of parkinsonism, where expression of SP mRNA is decreased and met-enk mRNA increased. Possible explanations include: (1) compensatory mechanisms, which may develop during the long term evolution of Parkinson's disease; (2) normalized expression of the two genes resulting from chronic L-DOPA therapy.</div>
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