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Brain-derived neurotrophic factor increases survival and differentiated functions of rat septal cholinergic neurons in culture
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 156591
Author(s) Alderson, R F; Alterman, A L; Barde, Y A; Lindsay, R M
Author(s) at UniBasel Barde, Yves-Alain
Year 1990
Title Brain-derived neurotrophic factor increases survival and differentiated functions of rat septal cholinergic neurons in culture
Journal Neuron
Volume 5
Number 3
Pages / Article-Number 297-306
Keywords Acetylcholinesterase/metabolism; Animals; Brain/*metabolism; Brain-Derived Neurotrophic Factor; Cell Count; Cell Differentiation/drug effects; Cell Survival/drug effects; Cells; Cultured; Nerve Growth Factors/metabolism/pharmacology; Nerve Tissue Proteins/metabolism/*pharmacology; Neurons/enzymology/metabolism/*physiology; Parasympathetic Nervous System/cytology/*physiology; Rats; Receptors; Cell Surface/metabolism; Nerve Growth Factor; Septum Pellucidum/cytology/*physiology; Time Factors
Abstract Brain-derived neurotrophic factor (BDNF) was found to promote the survival of E17 rat embryo septal cholinergic neurons in culture, as assessed by a histochemical stain for acetylcholinesterase (AChE). A 2.4-fold increase in neuronal survival was achieved with 10 ng/ml BDNF. After initial deprivation of growth factor for 7 days, BDNF failed to bring about this increase, strongly suggesting that BDNF promotes cell survival and not just induction of AChE. BDNF was also found to increase the levels of cholinergic enzymes; choline acetyltransferase (ChAT) and AChE activities were increased by approximately 2-fold in the presence of 50 ng/ml BDNF. BDNF produced a 3-fold increase in the number of cells bearing the NGF receptor, as detected by the monoclonal antibody IgG-192. Although NGF had no additive effect with BDNF in terms of neuronal survival, suggesting that both act on a similar neuronal population, the combination of both produced an additive response, approximately a 6-fold increase, in ChAT activity.
Publisher Cell Press
ISSN/ISBN 0896-6273
edoc-URL http://edoc.unibas.ch/dok/A5259557
Full Text on edoc No
Digital Object Identifier DOI 10.1016/0896-6273(90)90166-D
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/2169269
ISI-Number WOS:A1990DZ27900007
Document type (ISI) Article
 
   

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