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The Journal of Neurophysiology Vol. 87 No. 3 March 2002, pp. 1515-1525
Copyright ©2002 by the American Physiological Society
Department of Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama 35294
Chattipakorn, Siriporn C. and
Lori L. McMahon.
Pharmacological Characterization of Glycine-Gated Chloride
Currents Recorded in Rat Hippocampal Slices. J. Neurophysiol. 87: 1515-1525, 2002. An inhibitory role
for strychnine-sensitive glycine-gated chloride channels (GlyRs) in
mature hippocampus has been overlooked, largely due to the
misconception that GlyR expression ceases early during development and
to few functional studies demonstrating their presence. As a result,
little is known regarding the physiological and pharmacological
properties of native GlyRs expressed by hippocampal neurons. In this
study, we used pharmacological tools and whole cell patch-clamp
recordings of CA1 pyramidal cells and interneurons in acutely prepared
hippocampal slices from 3- to 4-wk old rats to characterize these
understudied receptors. We show that glycine application to recorded
pyramidal cells and interneurons elicited strychnine-sensitive
chloride-mediated currents (Igly) that
did not completely desensitize in the continued presence of agonist but
reached a steady state at 45-60% of the peak amplitude. Additionally, the inhibitory amino acid, taurine, which has been shown to activate GlyRs in other systems, activated GlyRs expressed by both pyramidal cells and interneurons, although with much less potency than glycine, having an EC50 10-fold higher. To examine the
potential subunit composition of hippocampal GlyRs, we tested the
effect of the GABAA receptor antagonist,
picrotoxin, on Igly recorded from both cell types. At low micromolar concentrations of picrotoxin (
100 µM), which selectively block 
homomeric GlyRs,
Igly was partially attenuated in both
cell types, indicating that homomeric receptors are expressed by
pyramidal cells and interneurons. At picrotoxin concentrations 1 mM,
~10-20% of the whole cell current remained, suggesting that 
heteromeric GlyRs are also expressed because this subtype of GlyR is
relatively resistant to picrotoxin antagonism. Finally, we examined
whether hippocampal GlyRs are modulated by zinc. Consistent with
previous reports in other preparations, zinc elicited a bidirectional
modulation of GlyRs, with physiological zinc concentrations (1-100
µM) increasing whole cell currents and concentrations >100 µM
depressing them. Furthermore, the same concentration of zinc that
potentiates Igly suppressed currents mediated by the N-methyl-D-aspartate subtype of
the glutamate receptor. Thus we provide a pharmacological
characterization of native GlyRs expressed by both major neuron types
in hippocampus and show that these receptors can be activated by
taurine, an amino acid that is highly concentrated in hippocampus.
Furthermore, our data suggest that at least two GlyR subtypes are
present in hippocampus and that GlyR-mediated currents can be
potentiated by zinc at concentrations that suppress glutamate-mediated excitability.
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