EconPapers    
Economics at your fingertips  
 

The K+/Cl− co-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation

Claudio Rivera, Juha Voipio, John A. Payne, Eva Ruusuvuori, Hannele Lahtinen, Karri Lamsa, Ulla Pirvola, Mart Saarma and Kai Kaila ()
Additional contact information
Claudio Rivera: Department of Biosciences, Division of Animal Physiology
Juha Voipio: Department of Biosciences, Division of Animal Physiology
John A. Payne: University of California School of Medicine
Eva Ruusuvuori: Department of Biosciences, Division of Animal Physiology
Hannele Lahtinen: Department of Biosciences, Division of Animal Physiology
Karri Lamsa: Department of Biosciences, Division of Animal Physiology
Ulla Pirvola: Institute of Biotechnology, Viikki Biocenter, University of Helsinki
Mart Saarma: Institute of Biotechnology, Viikki Biocenter, University of Helsinki
Kai Kaila: Department of Biosciences, Division of Animal Physiology

Nature, 1999, vol. 397, issue 6716, 251-255

Abstract: Abstract GABA (γ-aminobutyric acid) is the main inhibitory transmitter in the adult brain, and it exerts its fast hyperpolarizing effect through activation of anion (predominantly Cl−)-permeant GABAA receptors1. However, during early neuronal development, GABA A-receptor-mediated responses are often depolarizing2,3, which may be a key factor in the control of several Ca2+−dependent developmental phenomena, including neuronal proliferation, migration and targeting4,5,6. To date, however, the molecular mechanism underlying this shift in neuronal electrophysiological phenotype is unknown. Here we show that, in pyramidal neurons of the rat hippocampus, the ontogenetic change in GABAA-mediated responses from depolarizing to hyperpolarizing is coupled to a developmental induction of the expression of the neuronal Cl−-extruding K+/Cl− co-transporter, KCC2 (ref. 7). Antisense oligonucleotide inhibition of KCC2 expression produces a marked positive shift in the reversal potential of GABAA responses in functionally mature hippocampal pyramidal neurons. These data support the conclusion that KCC2 is the main Cl− extruder to promote fast hyperpolarizing postsynaptic inhibition in the brain.

Date: 1999
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/16697 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:397:y:1999:i:6716:d:10.1038_16697

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/16697

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().

 
Page updated 2025-03-19
Handle: RePEc:nat:nature:v:397:y:1999:i:6716:d:10.1038_16697