JN Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

J Neurophysiol (November 23, 2005). doi:10.1152/jn.00996.2005
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
95/3/1843    most recent
00996.2005v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Neusch, C.
Right arrow Articles by Hulsmann, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Neusch, C.
Right arrow Articles by Hulsmann, S.
Submitted on September 21, 2005
Accepted on November 15, 2005

Lack of the Kir4.1 channel subunit abolishes K+ buffering properties of astrocytes in the ventral respiratory group: Impact on extracellular K+ regulation

Clemens Neusch, Nestoras Papadopoulos, Michael Muller, Iris Maletzki, Stefan M. Winter, Johannes Hirrlinger, Melanie Handschuh, Mathias Bahr, Diethelm W. Richter, Frank Kirchhoff, and Swen Hulsmann*

* To whom correspondence should be addressed. E-mail: shuelsm2{at}uni-goettingen.de.

Rhythmic neuronal activity in the ventral respiratory group (VRG) of the brainstem results in periodic changes of extracellular K+. To estimate the involvement of the weakly inwardly rectifying K+ channel, Kir4.1 (KCNJ10), in extracellular K+ clearance, we examined its functional expression in astrocytes of the respiratory network. Kir4.1 was expressed in astroglial cells of the VRG, predominantly in fine astrocytic processes surrounding capillaries and in close proximity to VRG neurons. Kir4.1 expression was up-regulated during early postnatal development. The physiological role of astrocytic Kir4.1 was investigated using mice with a null mutation in the Kir4.1 channel gene that were interbred with transgenic mice expressing enhanced green fluorescent protein in their astrocytes. The membrane potential was depolarized in astrocytes in the VRG of Kir4.1-/- mice, and the activity of Ba2+-sensitive inward K+ currents was diminished. Brain slices containing the pre-Botzinger complex, which generate a respiratory rhythm, did not show any obvious differences in rhythmic bursting activity as compared to wild type controls, indicating that the lack of Kir4.1 channels alone does not impair respiratory network activity. Extracellular K+ measurements revealed that Kir4.1 channels contribute to extracellular K+ regulation. Kir4.1 channels reduce baseline K+ levels, and they compensate for the K+ undershoot. Our data indicate that Kir4.1 channels (i) are expressed in perineuronal processes of astrocytes, (ii) constitute the major part of the astrocytic K+ conductance and (iii) contribute to regulation of extracellular K+ in the respiratory network.




This article has been cited by other articles:


Home page
 J. Neurosci.Home page
J.-P. Vit, P. T. Ohara, A. Bhargava, K. Kelley, and L. Jasmin
Silencing the Kir4.1 Potassium Channel Subunit in Satellite Glial Cells of the Rat Trigeminal Ganglion Results in Pain-Like Behavior in the Absence of Nerve Injury
J. Neurosci., April 16, 2008; 28(16): 4161 - 4171.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
B. Djukic, K. B. Casper, B. D. Philpot, L.-S. Chin, and K. D. McCarthy
Conditional Knock-Out of Kir4.1 Leads to Glial Membrane Depolarization, Inhibition of Potassium and Glutamate Uptake, and Enhanced Short-Term Synaptic Potentiation
J. Neurosci., October 17, 2007; 27(42): 11354 - 11365.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
M. L. Olsen, S. L. Campbell, and H. Sontheimer
Differential Distribution of Kir4.1 in Spinal Cord Astrocytes Suggests Regional Differences in K+ Homeostasis
J Neurophysiol, August 1, 2007; 98(2): 786 - 793.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
J. Blanz, M. Schweizer, M. Auberson, H. Maier, A. Muenscher, C. A. Hubner, and T. J. Jentsch
Leukoencephalopathy upon Disruption of the Chloride Channel ClC-2
J. Neurosci., June 13, 2007; 27(24): 6581 - 6589.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2005 by the The American Physiological Society.