Document Detail

Neurotrophin regulation of ionic currents and cell size depends on cell context.
MedLine Citation:
PMID:  9159175     Owner:  NLM     Status:  MEDLINE    
Trk receptor activation by neurotrophins is often considered to have a defined set of actions on target neurons, including supporting neuronal survival, inducing morphological differentiation, and regulating a host of target genes that specify neuronal phenotype. It is not known if all such regulatory effects are obligatory, or if some may vary depending on the cell context in which the receptors are expressed. We have examined this issue by comparing neurotrophin effects on the regulation of electrical excitability and morphological differentiation in two strains of PC12 cells. We found that while neurotrophins induced neurite extension and increased calcium currents in both PC12 cell types, sodium current levels were regulated in only one of these strains. Moreover, we found little correlation between calcium current levels and the extent of morphological differentiation when compared in individual cells of a single strain. Thus, the regulatory effects of neurotrophins on cell phenotype are not fully determined by the Trk receptors that they activate; rather, they can vary with differences in cell context that arise not only between different cell lineages, but also between individual cells of clonal relation.
N T Sherwood; S S Lesser; D C Lo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  94     ISSN:  0027-8424     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  1997 May 
Date Detail:
Created Date:  1997-06-19     Completed Date:  1997-06-19     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  5917-22     Citation Subset:  IM    
Department of Neurobiology, Box 3209, Duke University Medical Center, Durham, NC 27710, USA.
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MeSH Terms
Calcium / metabolism
Calcium Channels / drug effects,  physiology
Membrane Potentials / drug effects
Nerve Growth Factors / pharmacology*
Neurites / drug effects,  physiology
PC12 Cells
Receptor Protein-Tyrosine Kinases / biosynthesis,  physiology*
Receptor, Ciliary Neurotrophic Factor
Receptor, trkC / biosynthesis,  physiology*
Receptors, Nerve Growth Factor / biosynthesis,  physiology*
Recombinant Proteins / metabolism
Sodium / metabolism
Sodium Channels / drug effects,  physiology
Grant Support
Reg. No./Substance:
0/Calcium Channels; 0/Nerve Growth Factors; 0/Receptor, Ciliary Neurotrophic Factor; 0/Receptors, Nerve Growth Factor; 0/Recombinant Proteins; 0/Sodium Channels; 7440-23-5/Sodium; 7440-70-2/Calcium; EC Protein-Tyrosine Kinases; EC, trkC

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