Dendrite Elongation and Dendritic Branching Are Affected Separately by Different Forms of Intrinsic Motoneuron Excitability
- Publikationstyp:
- Zeitschriftenaufsatz
- Metadaten:
-
- Autoren
- Carsten Duch
- Fernando Vonhoff
- Stefanie Ryglewski
- Autoren-URL
- https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=fis-test-1&SrcAuth=WosAPI&KeyUT=WOS:000260795600008&DestLinkType=FullRecord&DestApp=WOS_CPL
- DOI
- 10.1152/jn.90758.2008
- eISSN
- 1522-1598
- Externe Identifier
- Clarivate Analytics Document Solution ID: 370XE
- PubMed Identifier: 18715893
- ISSN
- 0022-3077
- Ausgabe der Veröffentlichung
- 5
- Zeitschrift
- JOURNAL OF NEUROPHYSIOLOGY
- Paginierung
- 2525 - 2536
- Datum der Veröffentlichung
- 2008
- Status
- Published
- Titel
- Dendrite Elongation and Dendritic Branching Are Affected Separately by Different Forms of Intrinsic Motoneuron Excitability
- Sub types
- Article
- Ausgabe der Zeitschrift
- 100
Datenquelle: Web of Science (Lite)
- Andere Metadatenquellen:
-
- Abstract
- <jats:p>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.</jats:p>
- Autoren
- Carsten Duch
- Fernando Vonhoff
- Stefanie Ryglewski
- DOI
- 10.1152/jn.90758.2008
- eISSN
- 1522-1598
- ISSN
- 0022-3077
- Ausgabe der Veröffentlichung
- 5
- Zeitschrift
- Journal of Neurophysiology
- Sprache
- en
- Paginierung
- 2525 - 2536
- Datum der Veröffentlichung
- 2008
- Status
- Published
- Herausgeber
- American Physiological Society
- Herausgeber URL
- http://dx.doi.org/10.1152/jn.90758.2008
- Datum der Datenerfassung
- 2021
- Titel
- Dendrite Elongation and Dendritic Branching Are Affected Separately by Different Forms of Intrinsic Motoneuron Excitability
- Ausgabe der Zeitschrift
- 100
Datenquelle: Crossref
- Abstract
- 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.
- Addresses
- School of Life Sciences, Arizona State University, Tempe, AZ 85287, USA. Carsten.duch@asu.edu
- Autoren
- Carsten Duch
- Fernando Vonhoff
- Stefanie Ryglewski
- DOI
- 10.1152/jn.90758.2008
- eISSN
- 1522-1598
- Externe Identifier
- PubMed Identifier: 18715893
- Open access
- false
- ISSN
- 0022-3077
- Ausgabe der Veröffentlichung
- 5
- Zeitschrift
- Journal of neurophysiology
- Schlüsselwörter
- Ganglia, Invertebrate
- Dendrites
- Motor Neurons
- Animals
- Animals, Newborn
- Animals, Genetically Modified
- Drosophila melanogaster
- Drosophila Proteins
- Green Fluorescent Proteins
- Transcription Factors
- Patch-Clamp Techniques
- Analysis of Variance
- Electric Stimulation
- Behavior, Animal
- Motor Activity
- Dose-Response Relationship, Radiation
- Membrane Potentials
- Locomotion
- Female
- Male
- Shaker Superfamily of Potassium Channels
- In Vitro Techniques
- CD8 Antigens
- Sprache
- eng
- Medium
- Print-Electronic
- Online publication date
- 2008
- Paginierung
- 2525 - 2536
- Datum der Veröffentlichung
- 2008
- Status
- Published
- Datum der Datenerfassung
- 2008
- Titel
- Dendrite elongation and dendritic branching are affected separately by different forms of intrinsic motoneuron excitability.
- Sub types
- Research Support, Non-U.S. Gov't
- Journal Article
- Ausgabe der Zeitschrift
- 100
Datenquelle: Europe PubMed Central
- Abstract
- 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.
- Autoren
- Carsten Duch
- Fernando Vonhoff
- Stefanie Ryglewski
- Autoren-URL
- https://www.ncbi.nlm.nih.gov/pubmed/18715893
- DOI
- 10.1152/jn.90758.2008
- ISSN
- 0022-3077
- Ausgabe der Veröffentlichung
- 5
- Zeitschrift
- J Neurophysiol
- Schlüsselwörter
- Analysis of Variance
- Animals
- Animals, Genetically Modified
- Animals, Newborn
- Behavior, Animal
- CD8 Antigens
- Dendrites
- Dose-Response Relationship, Radiation
- Drosophila Proteins
- Drosophila melanogaster
- Electric Stimulation
- Female
- Ganglia, Invertebrate
- Green Fluorescent Proteins
- In Vitro Techniques
- Locomotion
- Male
- Membrane Potentials
- Motor Activity
- Motor Neurons
- Patch-Clamp Techniques
- Shaker Superfamily of Potassium Channels
- Transcription Factors
- Sprache
- eng
- Country
- United States
- Paginierung
- 2525 - 2536
- PII
- 90758.2008
- Datum der Veröffentlichung
- 2008
- Status
- Published
- Datum, an dem der Datensatz öffentlich gemacht wurde
- 2009
- Titel
- Dendrite elongation and dendritic branching are affected separately by different forms of intrinsic motoneuron excitability.
- Sub types
- Journal Article
- Research Support, Non-U.S. Gov't
- Ausgabe der Zeitschrift
- 100
Datenquelle: PubMed
- Beziehungen:
- Eigentum von