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J. Biol. Chem., Vol. 278, Issue 7, 5317-5324, February 14, 2003
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From the Na,K-ATPase is an ion transporter that
impacts neural and glial physiology by direct electrogenic activity and
the modulation of ion gradients. Its three isoforms in brain have
cell-type and development-specific expression patterns. Interestingly,
our studies demonstrate that in late gestation, the
The Na,K-ATPase
2 Isoform Is Expressed in Neurons, and Its
Absence Disrupts Neuronal Activity in Newborn Mice*
,
,,
Department of Molecular Genetics,
Biochemistry, and Microbiology, the ** Department of
Pharmacology and Cell Biophysics, the *** Department of
Molecular and Cellular Physiology, and the
Department of Pathology and Laboratory
Medicine, University of Cincinnati, College of Medicine, Cincinnati,
Ohio 45267, the ¶ Laboratory of Membrane Biology, Neuroscience
Center, Massachusetts General Hospital, Charlestown, Massachusetts
02129, the Department of Zoology, Miami University, Oxford, Ohio
45056, the § Committee on Neurobiology and the
¶¶ Department of Organismal Biology and Anatomy, The
University of Chicago, Chicago, Illinois 60637, and the
§§ Department of Pathology, Children's
Hospital Medical Center, Cincinnati, Ohio 45229
2 isoform is
widely expressed in neurons, unlike in the adult brain, in which 2
has been shown to be expressed primarily in astrocytes. This unexpected
distribution of 2 isoform expression in neurons is interesting in
light of our examination of mice lacking the 2 isoform which fail to
survive after birth. These animals showed no movement; however, defects in gross brain development, muscle contractility, neuromuscular transmission, and lung development were ruled out. Akinesia suggests a
primary neuronal defect and electrophysiological recordings in the
pre-Bötzinger complex, the brainstem breathing center, showed
reduction of respiratory rhythm activity, with less regular and smaller
population bursts. These data demonstrate that the Na,K-ATPase 2
isoform could be important in the modulation of neuronal activity in
the neonate.
*
This work was supported by National Institutes of Health
Grants HL28573 and HL66062 (to J. B L.), NS27653 (to K. J. S.), and HL 60120 (to J. M. R.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of
Molecular Genetics, Biochemistry, and Microbiology, University of
Cincinnati, College of Medicine, 231 Albert Sabin Way, MSB Bldg., M.L.
0524, Cincinnati, OH 45267. Tel.: 513-558-5324; Fax:
513-558-8474; E-mail: jerry.lingrel@uc.edu.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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