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LIS1-dependent retrograde translocation of excitatory synapses in developing interneuron dendrites.
- Source :
-
Nature communications [Nat Commun] 2012 Mar 06; Vol. 3, pp. 722. Date of Electronic Publication: 2012 Mar 06. - Publication Year :
- 2012
-
Abstract
- Synaptic remodelling coordinated with dendritic growth is essential for proper development of neural connections. After establishment of synaptic contacts, synaptic junctions are thought to become stationary and provide fixed anchoring points for further dendritic growth. However, the possibility of active translocation of synapses along dendritic protrusions, to guide the proper arrangement of synaptic distribution, has not yet been fully investigated. Here we show that immature dendrites of γ-aminobutyric acid-positive interneurons form long protrusions and that these protrusions serve as conduits for retrograde translocation of synaptic contacts to the parental dendrites. This translocation process is dependent on microtubules and the activity of LIS1, an essential regulator of dynein-mediated motility. Suppression of this retrograde translocation results in disorganized synaptic patterns on interneuron dendrites. Taken together, these findings suggest the existence of an active microtubule-dependent mechanism for synaptic translocation that helps in the establishment of proper synaptic distribution on dendrites.
- Subjects :
- 1-Alkyl-2-acetylglycerophosphocholine Esterase genetics
Aminobutyrates
Animals
Cells, Cultured
Dendrites ultrastructure
Dyneins metabolism
Interneurons ultrastructure
Mice
Microtubule-Associated Proteins genetics
Microtubules physiology
Mutation
Post-Synaptic Density physiology
Post-Synaptic Density ultrastructure
Pseudopodia physiology
Pseudopodia ultrastructure
RNA Interference
RNA, Small Interfering
1-Alkyl-2-acetylglycerophosphocholine Esterase metabolism
Dendrites physiology
Interneurons physiology
Microtubule-Associated Proteins metabolism
Synapses physiology
Synaptic Transmission
Subjects
Details
- Language :
- English
- ISSN :
- 2041-1723
- Volume :
- 3
- Database :
- MEDLINE
- Journal :
- Nature communications
- Publication Type :
- Academic Journal
- Accession number :
- 22395613
- Full Text :
- https://doi.org/10.1038/ncomms1736