HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ransom, C. B. Articles by Sontheimer, H. Search for Related Content PubMed PubMed Citation Articles by Ransom, C. B. Articles by Sontheimer, H.

Activity-dependent extracellular K⁺ accumulation in rat optic nerve: the role of glial and axonal Na⁺ pumps

Christopher B. Ransom *, Bruce R. Ransom¹ and Harald Sontheimer *

1. We measured activity-dependent changes in [K⁺]_o with K⁺-selective microelectrodes in adult rat optic nerve, a CNS white matter tract, to investigate the factors responsible for post-stimulus recovery of [K⁺]_o.

2. Post-stimulus recovery of [K⁺]_o followed a double-exponential time course with an initial, fast time constant, _fast, of 0·9 ± 0·2 s (mean ± s.d.) and a later, slow time constant, _slow, of 4·2 ± 1 s following a 1 s, 100 Hz stimulus. _fast, but not _slow, decreased with increasing activity-dependent rises in [K⁺]_o. _slow, but not _fast, increased with increasing stimulus duration.

3. Post-stimulus recovery of [K⁺]_o was temperature sensitive. The apparent temperature coefficients (Q₁₀, 27-37°C) for the fast and slow components following a 1 s, 100 Hz stimulus were 1·7 and 2·6, respectively.

4. Post-stimulus recovery of [K⁺]_o was sensitive to Na⁺ pump inhibition with 50 µM strophanthidin. Following a 1 s, 100 Hz stimulus, 50 µM strophanthidin increased _fast and _slow by 81 and 464 %, respectively. Strophanthidin reduced the temperature sensitivity of post-stimulus recovery of [K⁺]_o.

5. Post-stimulus recovery of [K⁺]_o was minimally affected by the K⁺ channel blocker Ba²⁺ (0·2 mM). Following a 10 s, 100 Hz stimulus, 0·2 mM Ba²⁺ increased _fast and _slow by 24 and 18 %, respectively.

6. Stimulated increases in [K⁺]_o were followed by undershoots of [K⁺]_o. Post-stimulus undershoot amplitude increased with stimulus duration but was independent of the peak preceding [K⁺]_o increase.

7. These observations imply that two distinct processes contribute to post-stimulus recovery of [K⁺]_o in central white matter. The results are compatible with a model of K⁺ removal that attributes the fast, initial phase of K⁺ removal to K⁺ uptake by glial Na⁺ pumps and the slower, sustained decline to K⁺ uptake via axonal Na⁺ pumps.

This article has been cited by other articles:

				J. L. Orthmann-Murphy, M. Freidin, E. Fischer, S. S. Scherer, and C. K. Abrams Two Distinct Heterotypic Channels Mediate Gap Junction Coupling between Astrocyte and Oligodendrocyte Connexins J. Neurosci., December 19, 2007; 27(51): 13949 - 13957. [Abstract] [Full Text] [PDF]

				D. M. Menichella, M. Majdan, R. Awatramani, D. A. Goodenough, E. Sirkowski, S. S. Scherer, and D. L. Paul Genetic and Physiological Evidence That Oligodendrocyte Gap Junctions Contribute to Spatial Buffering of Potassium Released during Neuronal Activity J. Neurosci., October 25, 2006; 26(43): 10984 - 10991. [Abstract] [Full Text] [PDF]

				A. Wallraff, R. Kohling, U. Heinemann, M. Theis, K. Willecke, and C. Steinhauser The impact of astrocytic gap junctional coupling on potassium buffering in the hippocampus. J. Neurosci., May 17, 2006; 26(20): 5438 - 5447. [Abstract] [Full Text] [PDF]

				L. Segall, R. Scanzano, M. A. Kaunisto, M. Wessman, A. Palotie, J. J. Gargus, and R. Blostein Kinetic Alterations due to a Missense Mutation in the Na,K-ATPase {alpha}2 Subunit Cause Familial Hemiplegic Migraine Type 2 J. Biol. Chem., October 15, 2004; 279(42): 43692 - 43696. [Abstract] [Full Text] [PDF]

				A. E. Moseley, S. P. Lieske, R. K. Wetzel, P. F. James, S. He, D. A. Shelly, R. J. Paul, G. P. Boivin, D. P. Witte, J. M. Ramirez, et al. The Na,K-ATPase alpha 2 Isoform Is Expressed in Neurons, and Its Absence Disrupts Neuronal Activity in Newborn Mice J. Biol. Chem., February 7, 2003; 278(7): 5317 - 5324. [Abstract] [Full Text] [PDF]

				R. D'Ambrosio, D. S. Gordon, and H. R. Winn Differential Role of KIR Channel and Na+/K+-Pump in the Regulation of Extracellular K+ in Rat Hippocampus J Neurophysiol, January 1, 2002; 87(1): 87 - 102. [Abstract] [Full Text] [PDF]

				I. A. Fleidervish, C. Gebhardt, N. Astman, M. J. Gutnick, and U. Heinemann Enhanced Spontaneous Transmitter Release Is the Earliest Consequence of Neocortical Hypoxia That Can Explain the Disruption of Normal Circuit Function J. Neurosci., July 1, 2001; 21(13): 4600 - 4608. [Abstract] [Full Text] [PDF]

				R. A. DeFazio, S. Keros, M. W. Quick, and J. J. Hablitz Potassium-Coupled Chloride Cotransport Controls Intracellular Chloride in Rat Neocortical Pyramidal Neurons J. Neurosci., November 1, 2000; 20(21): 8069 - 8076. [Abstract] [Full Text] [PDF]

				H. Dong, P. E. Light, R. J. French, and J. Lytton Electrophysiological Characterization and Ionic Stoichiometry of the Rat Brain K+-dependent Na+/Ca2+ Exchanger, NCKX2 J. Biol. Chem., July 6, 2001; 276(28): 25919 - 25928. [Abstract] [Full Text] [PDF]