Please use this identifier to cite or link to this item: https://doi.org/10.7554/eLife.20770
Title: Thalamo-cortical axons regulate the radial dispersion of neocortical GABAergic interneurons
Authors: Zechel, S
Nakagawa, Y
Ibáñez, C.F 
Keywords: 4 aminobutyric acid receptor
calpain
calpastatin
glutamic acid
n methyl dextro aspartic acid receptor
potassium chloride cotransporter 2
tamoxifen
4 aminobutyric acid receptor
animal tissue
Article
axon
brain cortex layer
cell migration
confocal microscopy
controlled study
denervation
electroporation
embryo
female
GABAergic system
image analysis
immunofluorescence test
immunohistochemistry
in situ hybridization
interneuron
mouse
neocortex
newborn
nonhuman
orientation
polymerase chain reaction
protein expression
radial dispersion
RNA probe
tangential orientation
thalamocortical tract
upregulation
animal
axon
brain cortex
cell motion
embryology
interneuron
nerve tract
physiology
thalamus
Animals
Axons
Cell Movement
Cerebral Cortex
GABAergic Neurons
Interneurons
Mice
Neural Pathways
Thalamus
Issue Date: 2016
Citation: Zechel, S, Nakagawa, Y, Ibáñez, C.F (2016). Thalamo-cortical axons regulate the radial dispersion of neocortical GABAergic interneurons. eLife 5 (42705) : e20770. ScholarBank@NUS Repository. https://doi.org/10.7554/eLife.20770
Abstract: Neocortical GABAergic interneuron migration and thalamo-cortical axon (TCA) pathfinding follow similar trajectories and timing, suggesting they may be interdependent. The mechanisms that regulate the radial dispersion of neocortical interneurons are incompletely understood. Here we report that disruption of TCA innervation, or TCA-derived glutamate, affected the laminar distribution of GABAergic interneurons in mouse neocortex, resulting in abnormal accumulation in deep layers of interneurons that failed to switch from tangential to radial orientation. Expression of the KCC2 cotransporter was elevated in interneurons of denervated cortex, and KCC2 deletion restored normal interneuron lamination in the absence of TCAs. Disruption of interneuron NMDA receptors or pharmacological inhibition of calpain also led to increased KCC2 expression and defective radial dispersion of interneurons. Thus, although TCAs are not required to guide the tangential migration of GABAergic interneurons, they provide crucial signals that restrict interneuron KCC2 levels, allowing coordinated neocortical invasion of TCAs and interneurons. © Zechel et al.
Source Title: eLife
URI: https://scholarbank.nus.edu.sg/handle/10635/173976
ISSN: 2050084X
DOI: 10.7554/eLife.20770
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