Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 19, Pages 5224-5235Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5169-06.2007
Keywords
KCC2; development; radial migration; K(ir)2.1; in utero electroporation; gramicidin perforated-patch
Categories
Funding
- NINDS NIH HHS [R01 NS036999, NS36999] Funding Source: Medline
Ask authors/readers for more resources
GABA exerts excitatory actions on embryonic and neonatal cortical neurons, but the in vivo function of this GABA excitation is essentially unknown. Using in utero electroporation, we eliminated the excitatory action of GABA in a subpopulation of rat ventricular progenitors and cortical neurons derived from these progenitors by premature expression of the Cl- transporter KCC2, as confirmed by the changes in the reversal potential of GABA-induced currents and the resting membrane potential after GABAA receptor blockade. We found that radial migration to layer II/III of the somatosensory cortex of neurons derived from the transfected progenitors was not significantly affected, but their morphological maturation was markedly impaired. Furthermore, reducing neuronal excitability of cortical neurons in vivo by overexpressing an inward-rectifying K+ channel, which lowered the resting membrane potential, mimicked the effect of premature KCC2 expression. Thus, membrane depolarization caused by early GABA excitation is critical for morphological maturation of neonatal cortical neurons in vivo.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available