Document Detail


TrkB downregulation is required for dendrite retraction in developing neurons of chicken nucleus magnocellularis.
MedLine Citation:
PMID:  23035107     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The chick embryo (Gallus domesticus) is one of the most important model systems in vertebrate developmental biology. The development and function of its auditory brainstem circuitry is exceptionally well studied. These circuits represent an excellent system for genetic manipulation to investigate mechanisms controlling neural circuit formation, synaptogenesis, neuronal polarity, and dendritic arborization. The present study investigates the auditory nucleus, nucleus magnocellularis (NM). The neurotrophin receptor TrkB regulates dendritic structure in CNS neurons. TrkB is expressed in NM neurons at E7-E8 when these neurons have dendritic arbors. Downregulation of TrkB occurs after E8 followed by retraction of dendrites and by E18 most NM cells are adendritic. Is cessation of TrkB expression in NM necessary for dendritic retraction? To answer this question we combined focal in ovo electroporation with transposon mediated gene transfer to obtain stable expression of Doxycycline (Dox) regulated transgenes, specifically TrkB coexpressed with EGFP in a temporally controlled manner. Electroporation was performed at E2 and Dox added onto the chorioallointoic membrane from E7.5 to E16. Expression of EGFP had no effect on development of the embryo, or cell morphology and organization of auditory brainstem nuclei. NM cells expressing EGFP and TrkB at E17-E18 had dendrites and biophysical properties uncharacteristic for normal NM cells, indicating that cessation of TrkB expression is essential for dendrite retraction and functional maturation of these neurons. These studies indicate that expression of transposon based plasmids is an effective method to genetically manipulate events in mid to late embryonic brain development in chick.
Authors:
Leslayann C Schecterson; Jason Tait Sanchez; Edwin W Rubel; Mark Bothwell
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  The Journal of neuroscience : the official journal of the Society for Neuroscience     Volume:  32     ISSN:  1529-2401     ISO Abbreviation:  J. Neurosci.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-04     Completed Date:  2013-01-17     Revised Date:  2013-07-11    
Medline Journal Info:
Nlm Unique ID:  8102140     Medline TA:  J Neurosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  14000-9     Citation Subset:  IM    
Affiliation:
Institute for Stem Cell and Regenerative Medicine and Department of Physiology and Biophysics, University of Washington, Seattle, Washington 98109, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Auditory Pathways / embryology*
Brain Stem / embryology*
Chick Embryo
DNA Transposable Elements / genetics
Dendrites / physiology*
Down-Regulation
Doxycycline / pharmacology
Electroporation
Female
Gene Expression Regulation, Developmental* / drug effects
Genes, Reporter
Green Fluorescent Proteins / biosynthesis,  genetics
Male
Neurogenesis / genetics,  physiology*
Neurons / cytology,  metabolism*
Receptor, trkB / biosynthesis,  genetics,  physiology*
Recombinant Fusion Proteins / biosynthesis,  physiology
Transgenes
Grant Support
ID/Acronym/Agency:
R01 DC003829/DC/NIDCD NIH HHS; R01 DC003829/DC/NIDCD NIH HHS; R21 DC011504/DC/NIDCD NIH HHS; R21 DC011594/DC/NIDCD NIH HHS
Chemical
Reg. No./Substance:
0/DNA Transposable Elements; 0/Recombinant Fusion Proteins; 0/enhanced green fluorescent protein; 147336-22-9/Green Fluorescent Proteins; 564-25-0/Doxycycline; EC 2.7.10.1/Receptor, trkB
Comments/Corrections

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


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