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PMID: 10226934 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Midbrain dopaminergic neurons are protected from radical induced damage by GDF-5 application. Short communication.

Journal of neural transmission (Vienna, Austria : 1996) ·Vol. 106 ·No. 2 ·1999-00-00 ·Pages 139-44

Lingor P, Unsicker K, Krieglstein K

Abstract

Embryonic day 14 rat midbrain cultures were kept for 7 days in vitro and then intoxicated with radical donors iron and sodium-nitroprusside for 24 h. Tyrosine-hydroxylase positive neurons in cultures which were additionally treated with growth/differentiation factor-5 (GDF-5) survived to a significantly higher percentage as compared to sister cultures without factor supplementation. Since the degeneration of TH positive cells is a key feature in Parkinson's disease, GDF-5 might be a putative therapeutical agent for this disorder.

MeSH Terms
Animals Apoptosis/drug effects Bone Morphogenetic Proteins Cell Survival/drug effects Cells, Cultured Dopamine/metabolism Dose-Response Relationship, Drug Ferrous Compounds/toxicity Free Radicals/toxicity Growth Differentiation Factor 5 Growth Substances/pharmacology,therapeutic use Lethal Dose 50 Mesencephalon/cytology,embryology Neurons/cytology,drug effects,metabolism Nitric Oxide Donors/pharmacology Nitroprusside/pharmacology Parkinson Disease/drug therapy Rats Rats, Wistar Tyrosine 3-Monooxygenase/metabolism
Chemicals
Bone Morphogenetic Proteins Ferrous Compounds Free Radicals Growth Differentiation Factor 5 Growth Substances Nitric Oxide Donors Nitroprusside Tyrosine 3-Monooxygenase ferrous chloride Dopamine
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Lingor P
University of Heidelberg, Federal Republic of Germany.
Unsicker K
Krieglstein K
Article Info
Journal
Journal of neural transmission (Vienna, Austria : 1996)
Abbr.
J Neural Transm (Vienna)
ISSN
0300-9564
DOI
10.1007/s007020050146
Published
1999-00-00
Pages
139-44
Language
English
Region
Austria
NLM ID
9702341
Subset
IM
External Links
PubMed source DOI: 10.1007/s007020050146 View journal details
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