Document Detail


Dendrite elongation and dendritic branching are affected separately by different forms of intrinsic motoneuron excitability.
MedLine Citation:
PMID:  18715893     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Dendrites are the fundamental determinant of neuronal wiring. Consequently dendritic defects are associated with numerous neurological diseases and mental retardation. Neuronal activity can have profound effects on dendritic structure, but the mechanisms controlling distinct aspects of dendritic architecture are not fully understood. We use the Drosophila genetic model system to test the effects of altered intrinsic excitability on postembryonic dendritic architecture development. Targeted dominant negative knock-downs of potassium channel subunits allow for selectively increasing the intrinsic excitability of a selected subset of motoneurons, whereas targeted expression of a genetically modified noninactivating potassium channel decrease intrinsic excitability in vivo. Both manipulations cause significant dendritic overgrowth, but by different mechanisms. Increased excitability causes increased dendritic branch formation, whereas decreased excitability causes increased dendritic branch elongation. Therefore dendritic branching and branch elongation are controlled by separate mechanisms that can be addressed selectively in vivo by different manipulations of neuronal intrinsic excitability.
Authors:
Carsten Duch; Fernando Vonhoff; Stefanie Ryglewski
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-08-20
Journal Detail:
Title:  Journal of neurophysiology     Volume:  100     ISSN:  0022-3077     ISO Abbreviation:  J. Neurophysiol.     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-11-12     Completed Date:  2009-04-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375404     Medline TA:  J Neurophysiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2525-36     Citation Subset:  IM    
Affiliation:
School of Life Sciences, Arizona State University, Tempe, AZ 85287, USA. Carsten.duch@asu.edu
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Animals, Genetically Modified
Animals, Newborn
Antigens, CD8 / genetics,  metabolism
Behavior, Animal
Dendrites / drug effects,  physiology*,  radiation effects
Dose-Response Relationship, Radiation
Drosophila Proteins / genetics,  metabolism
Drosophila melanogaster
Electric Stimulation
Female
Ganglia, Invertebrate / cytology
Green Fluorescent Proteins / biosynthesis,  genetics
Locomotion / genetics
Male
Membrane Potentials / drug effects,  physiology,  radiation effects
Motor Activity / genetics
Motor Neurons / classification*,  cytology*,  physiology
Patch-Clamp Techniques
Shaker Superfamily of Potassium Channels / genetics,  metabolism
Transcription Factors / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Antigens, CD8; 0/Drosophila Proteins; 0/Shaker Superfamily of Potassium Channels; 0/Shaker protein, Drosophila; 0/Transcription Factors; 147336-22-9/Green Fluorescent Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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