JN Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Neurophysiol 82: 768-777, 1999;
0022-3077/99 $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 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 Web of Science (23)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Perkins, K. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Perkins, K. L.

The Journal of Neurophysiology Vol. 82 No. 2 August 1999, pp. 768-777
Copyright ©1999 by the American Physiological Society

Clminus Accumulation Does Not Account for the Depolarizing Phase of the Synaptic GABA Response in Hippocampal Pyramidal Cells

Katherine L. Perkins

Department of Physiology and Pharmacology, State University of New York Health Science Center, Brooklyn, New York 11203

Perkins, Katherine L. Clminus Accumulation Does Not Account for the Depolarizing Phase of the Synaptic GABA Response in Hippocampal Pyramidal Cells. J. Neurophysiol. 82: 768-777, 1999. It has been proposed that the depolarizing phase of the biphasic synaptic GABA response could be mediated by HCO3- passing through GABAA channels after dissipation of the transmembrane Cl- gradient due to intracellular Cl- accumulation. To test this hypothesis, giant GABA-mediated postsynaptic currents (GPSCs) were recorded from pyramidal cells in slices of adult guinea pig hippocampus in the presence of 4-aminopyridine. GPSCs consisted of an early outward current (GABAA component) followed by a late inward current (GABAD component). Spontaneous outward inhibitory postsynaptic currents (IPSCs) occurred during the GABAD component of the GPSC. GPSCs that were evoked 1-12 s after the preceding GPSC (short interval, siGPSCs) showed no GABAD component even though in many cells the amplitude of the siGPSC was greater than the amplitude of the GABAA component of the preceding spontaneous GPSC. In addition, the siGPSC evoked during the GABAD component of a spontaneous GPSC was an outward current. To test whether the siGPSC lacked a GABAD component because it was generated predominantly at the soma, where less of an increase in [Cl-]i would occur, picrotoxin was applied to the soma of the pyramidal cell. To the contrary, this focal application of picrotoxin caused less of a reduction in the amplitude of the siGPSC than in the amplitude of the GABAA component of the GPSC. Furthermore when a GPSC and siGPSC were evoked 10 s apart using identical stimuli, the area under the outward current curve was sometimes greater for the siGPSC than for the GPSC, and yet the siGPSC had no inward component. This result indicates that even when the location of Cl- entry was the same, more Cl- could enter the cell during the siGPSC than during the outward component of the GPSC and yet not lead to an inward current. In addition, when the second of two identical stimuli was applied during the inward GABAD component of the first evoked GPSC, the GABAA response it generated was always outward, demonstrating that the equilibrium potential for GABAA responses did not become more positive than the holding potential during a GPSC. Finally, evoking GPSCs at a hyperpolarized potential revealed that the siGPSC actually lacked a GABAD conductance. These results disprove the Cl- accumulation hypothesis of the synaptic depolarizing GABA response and suggest the possibility that a separate channel type may mediate the GABAD component of the GPSC.




This article has been cited by other articles:


Home page
J. Physiol.Home page
V. Zsiros, I. Aradi, and G. Maccaferri
Propagation of postsynaptic currents and potentials via gap junctions in GABAergic networks of the rat hippocampus
J. Physiol., January 15, 2007; 578(2): 527 - 544.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
M. Cordero-Erausquin, J. A. M. Coull, D. Boudreau, M. Rolland, and Y. D. Koninck
Differential Maturation of GABA Action and Anion Reversal Potential in Spinal Lamina I Neurons: Impact of Chloride Extrusion Capacity
J. Neurosci., October 19, 2005; 25(42): 9613 - 9623.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
J. T. Kantrowitz, N. N. Francis, A. Salah, and K. L. Perkins
Synaptic Depolarizing GABA Response in Adults Is Excitatory and Proconvulsive When GABAB Receptors Are Blocked
J Neurophysiol, May 1, 2005; 93(5): 2656 - 2667.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
N. Kang, L. Jiang, W. He, J. Xu, M. Nedergaard, and J. Kang
Presynaptic Inactivation of Action Potentials and Postsynaptic Inhibition of GABAA Currents Contribute to KA-Induced Disinhibition in CA1 Pyramidal Neurons
J Neurophysiol, August 1, 2004; 92(2): 873 - 882.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
A. R. McQuiston and P. Saggau
Mu-opioid Receptors Facilitate the Propagation of Excitatory Activity in Rat Hippocampal Area CA1 by Disinhibition of all Anatomical Layers
J Neurophysiol, September 1, 2003; 90(3): 1936 - 1948.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
K. Lamsa and T. Taira
Use-Dependent Shift From Inhibitory to Excitatory GABAA Receptor Action in SP-O Interneurons in the Rat Hippocampal CA3 Area
J Neurophysiol, September 1, 2003; 90(3): 1983 - 1995.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
K. L. Perkins
GABA Application to Hippocampal CA3 or CA1 Stratum Lacunosum-Moleculare Excites an Interneuron Network
J Neurophysiol, March 1, 2002; 87(3): 1404 - 1414.
[Abstract] [Full Text] [PDF]


Home page
J. Physiol.Home page
J. F M Van Brederode, T. Takigawa, and C. Alzheimer
GABA-evoked chloride currents do not differ between dendrites and somata of rat neocortical neurons
J. Physiol., June 15, 2001; 533(3): 711 - 716.
[Abstract] [Full Text] [PDF]


Home page
J. Neurophysiol.Home page
P. R. Patrylo, D. D. Spencer, and A. Williamson
GABA Uptake and Heterotransport Are Impaired in the Dentate Gyrus of Epileptic Rats and Humans With Temporal Lobe Sclerosis
J Neurophysiol, April 1, 2001; 85(4): 1533 - 1542.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
R. Kohling, M. Vreugdenhil, E. Bracci, and J. G. R. Jefferys
Ictal Epileptiform Activity Is Facilitated by Hippocampal GABAA Receptor-Mediated Oscillations
J. Neurosci., September 15, 2000; 20(18): 6820 - 6829.
[Abstract] [Full Text] [PDF]


Home page
J. Neurosci.Home page
S. Smirnov, P. Paalasmaa, M. Uusisaari, J. Voipio, and K. Kaila
Pharmacological Isolation of the Synaptic and Nonsynaptic Components of the GABA-Mediated Biphasic Response in Rat CA1 Hippocampal Pyramidal Cells
J. Neurosci., November 1, 1999; 19(21): 9252 - 9260.
[Abstract] [Full Text] [PDF]




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