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J Physiol Volume 585, Number 2, 491-505, December 1, 2007 DOI: 10.1113/jphysiol.2007.144733
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NEUROSCIENCE

Differential expression of Na+/K+-ATPase {alpha}-subunits in mouse hippocampal interneurones and pyramidal cells

Kathryn S. Richards1, Kurt Bommert2, Gabor Szabo3 and Richard Miles1

1 INSERM U739, UPMC Paris VI CHU Pitié Salpêtrière, Paris, France
2 Medizinische Klinik und Poliklinik II, University of Würzburg, D-97070 Würzburg Germany
3 Laboratory of Molecular Biology and Genetics, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary

The sodium pump (Na+/K+-ATPase), maintains intracellular and extracellular concentrations of sodium and potassium by catalysing ATP. Three sodium pump {alpha} subunits, ATP1A1, ATP1A2 and ATP1A3, are expressed in brain. We compared their role in pyramidal cells and a subset of interneurones in the subiculum. Interneurones were identified by their expression of GFP under the GAD-65 promoter. We used the sensitivity to the cardiac glycoside, ouabain, to discriminate between different {alpha} subunit isoforms. GFP-positive interneurones were depolarized by nanomolar doses of ouabain, but higher concentrations were needed to depolarize pyramidal cells. Comparison of pump currents in these cells revealed a current sensitive to low doses of ouabain in interneurones, while micromolar doses of ouabain were needed to suppress the pump current in subicular pyramidal cells. As predicted, nanomolar doses of ouabain increased the frequency but not the amplitudes of IPSPs in pyramidal cells. Immunostaining confirmed a differential distribution of {alpha}-subunits of the Na+/K+-ATPase in subicular interneurones and pyramidal cells. In conclusion, these data suggest that while ATP1A3-isoforms regulate sodium and potassium homeostasis in subicular interneurones, ATP1A1-isoforms assume this function in pyramidal cells. This differential expression of sodium pump isoforms may contribute to differences in resting membrane potential of subicular interneurones and pyramidal cells.

(Received 7 September 2007; accepted after revision 10 October 2007; first published online 18 October 2007)
Corresponding author K. S. Richards: INSERM U739, CHU Pitié-Salpêtrière, 105 boulevard de l'Hôpital, 75013 Paris. Email: kat{at}chups.jussieu.fr


This paper has online supplemental material.







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