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Volume 17, Number 20,
Issue of October 15, 1997
pp. 7662-7672
Copyright ©1997 Society for Neuroscience
Long-Lasting GABA-Mediated Depolarization Evoked by
High-Frequency Stimulation in Pyramidal Neurons of Rat Hippocampal
Slice Is Attributable to a Network-Driven, Bicarbonate-Dependent
K+ Transient
Received May 12, 1997; revised July 21, 1997; accepted Aug. 5, 1997.
Kai Kaila,
Karri Lamsa,
Sergei Smirnov,
Tomi Taira, and
Juha Voipio
Department of Biosciences, Division of Animal Physiology,
University of Helsinki, FIN-00014 Helsinki, Finland
Biphasic GABAA-mediated postsynaptic responses can be
readily evoked in CA1 pyramidal neurons of rat hippocampal slices by high-frequency stimulus (HFS) trains in the presence of ionotropic glutamate receptor antagonists. In the present experiments with sharp
microelectrodes, whole-cell techniques, and
K+-selective microelectrodes, an HFS train (40 pulses at 100 Hz) applied in stratum radiatum close to the recording
site evoked a brief hyperpolarizing IPSP (hIPSP), which turned into a
prolonged (2-3 sec) depolarization ( ABA-mediated
 epolarizing  ostsynaptic otential; GDPSP). The I-V relationships of
the postsynaptic currents (hIPSC and GDPSC) had distinct
characteristics: the hIPSC and the early GDPSC showed outward
rectification, whereas the late GDPSC was reduced with positive voltage
steps to zero or beyond (inward rectification), but often no clear
reversal was seen. That two distinct currents contribute to the
generation of the GDPSP was also evident from the finding that a second
HFS train at peak or late GDPSP induced a prompt
GABAA-mediated hyperpolarization. The GDPSP/C was dependent
on the availability of bicarbonate, but not on interstitial or
intrapyramidal carbonic anhydrase activity.
The HFS train evoked a rapid GABAA-mediated
bicarbonate-dependent increase in the extracellular
K+ concentration
([K+]o), and the GDPSP followed
the K+ transient in a sub-Nernstian manner. The
spatial and pharmacological characteristics of the
[K+]o shift indicated that it is
generated by a local network of GABAergic interneurons. The brief
ascending phase of the GDPSP is linked to a
K+-dependent accumulation of intracellular
Cl . Thereafter, a nonsynaptic mechanism, a direct
depolarizing effect of the [K+]o
shift, is responsible for the most conspicuous characteristics of the
GDPSP: its large amplitude and prolonged duration.
Key words:
GABAA receptor;
postsynaptic depolarization;
bicarbonate;
potassium;
hippocampal pyramidal neuron;
inhibitory
network;
glial depolarization
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K. L. Perkins
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[Abstract]
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W. Jarolimek, A. Lewen, and U. Misgeld
A Furosemide-Sensitive K+-Cl- Cotransporter Counteracts Intracellular Cl- Accumulation and Depletion in Cultured Rat Midbrain Neurons
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M.-K. Sun, T. J. Nelson, H. Xu, and D. L. Alkon
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Y. Kakazu, N. Akaike, S. Komiyama, and J. Nabekura
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J. A. H. Verheugen, D. Fricker, and R. Miles
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A.-M. Autere, K. Lamsa, K. Kaila, and T. Taira
Synaptic Activation of GABAA Receptors Induces Neuronal Uptake of Ca2+ in Adult Rat Hippocampal Slices
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E. A. Barnard, P. Skolnick, R. W. Olsen, H. Mohler, W. Sieghart, G. Biggio, C. Braestrup, A. N. Bateson, and S. Z. Langer
International Union of Pharmacology. XV. Subtypes of gamma -Aminobutyric AcidA Receptors: Classification on the Basis of Subunit Structure and Receptor Function
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