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


     

J Neurophysiol 85: 1719-1731, 2001;
0022-3077/01 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 ISI Web of Science (38)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bordey, A.
Right arrow Articles by Sontheimer, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bordey, A.
Right arrow Articles by Sontheimer, H.

The Journal of Neurophysiology Vol. 85 No. 4 April 2001, pp. 1719-1731
Copyright ©2001 by the American Physiological Society

Electrophysiological Characteristics of Reactive Astrocytes in Experimental Cortical Dysplasia

A. Bordey, S. A. Lyons, J. J. Hablitz, and H. Sontheimer

Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294

Bordey, A., S. A. Lyons, J. J. Hablitz, and H. Sontheimer. Electrophysiological Characteristics of Reactive Astrocytes in Experimental Cortical Dysplasia. J. Neurophysiol. 85: 1719-1731, 2001. Neocortical freeze lesions have been widely used to study neuronal mechanisms underlying hyperexcitability in dysplastic cortex. Comparatively little attention has been given to biophysical changes in the surrounding astrocytes that show profound morphological and biochemical alterations, often referred to as reactive gliosis. Astrocytes are thought to aid normal neuronal function by buffering extracellular K+. Compromised astrocytic K+ buffering has been proposed to contribute to neuronal dysfunction. Astrocytic K+ buffering is mediated, partially, by the activity of inwardly rectifying K+ channels (KIR) and may involve intracellular redistribution of K+ through gap-junctions. We characterized K+ channel expression and gap-junction coupling between astrocytes in freeze-lesion-induced dysplastic neocortex. Whole cell patch-clamp recordings were obtained from astrocytes in slices from postnatal day (P) 16-P24 rats that had received a freeze-lesion on P1. A marked increase in glial fibrillary acidic protein immunoreactivity was observed along the entire length of the freeze lesion. Clusters of proliferative (bromo-deoxyuridine nuclear staining, BrdU+) astrocytes were seen near the depth of the microsulcus. Astrocytes in cortical layer I surrounding the lesion were characterized by a significant reduction in KIR. BrdU-positive astrocytes near the depth of the microsulcus showed essentially no expression of KIR channels but markedly enhanced expression of delayed rectifier K+ (KDR) channels. These proliferative cells showed virtually no dye coupling, whereas astrocytes in the hyperexcitable zone adjacent to the microsulcus displayed prominent dye-coupling as well as large KIR and outward K+ currents. These findings suggest that reactive gliosis is accompanied by a loss of KIR currents and reduced gap junction coupling, which in turn suggests a compromised K+ buffering capacity.




This article has been cited by other articles:


Home page
 BrainHome page
S. Ivens, D. Kaufer, L. P Flores, I. Bechmann, D. Zumsteg, O. Tomkins, E. Seiffert, U. Heinemann, and A. Friedman
TGF-{beta} receptor-mediated albumin uptake into astrocytes is involved in neocortical epileptogenesis
Brain, February 1, 2007; 130(2): 535 - 547.
[Abstract] [Full Text] [PDF]

Home page
 J Child NeurolHome page
A. Kakita, S. Kameyama, S. Hayashi, H. Masuda, and H. Takahashi
Pathologic Features of Dysplasia and Accompanying Alterations Observed in Surgical Specimens From Patients With Intractable Epilepsy
J Child Neurol, April 1, 2005; 20(4): 341 - 350.
[Abstract] [PDF]

Home page
 J. Neurosci.Home page
E. Seiffert, J. P. Dreier, S. Ivens, I. Bechmann, O. Tomkins, U. Heinemann, and A. Friedman
Lasting Blood-Brain Barrier Disruption Induces Epileptic Focus in the Rat Somatosensory Cortex
J. Neurosci., September 8, 2004; 24(36): 7829 - 7836.
[Abstract] [Full Text] [PDF]

Home page
 J Child NeurolHome page
A. Kakita, S. Kameyama, S. Hayashi, H. Masuda, and H. Takahashi
Pathologic Features of Dysplasia and Accompanying Alterations Observed in Surgical Specimens from Patients with Intractable Epilepsy
J Child Neurol, March 1, 2004; 19(3): 341 - 350.
[Abstract] [PDF]

Home page
 DevelopmentHome page
B. Scheffler, T. Schmandt, W. Schroder, B. Steinfarz, L. Husseini, J. Wellmer, G. Seifert, K. Karram, H. Beck, I. Blumcke, et al.
Functional network integration of embryonic stem cell-derived astrocytes in hippocampal slice cultures
Development, November 15, 2003; 130(22): 5533 - 5541.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
D. D. Wang, D. D. Krueger, and A. Bordey
Biophysical Properties and Ionic Signature of Neuronal Progenitors of the Postnatal Subventricular Zone In Situ
J Neurophysiol, October 1, 2003; 90(4): 2291 - 2302.
[Abstract] [Full Text] [PDF]

Home page
 NEJMHome page
B. S. Chang and D. H. Lowenstein
Epilepsy
N. Engl. J. Med., September 25, 2003; 349(13): 1257 - 1266.
[Full Text] [PDF]

Home page
 J. Neurosci.Home page
F. Amzica, M. Massimini, and A. Manfridi
Spatial Buffering during Slow and Paroxysmal Sleep Oscillations in Cortical Networks of Glial Cells In Vivo
J. Neurosci., February 1, 2002; 22(3): 1042 - 1053.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online