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The Journal of Neuroscience, February 15, 1998, 18(4):1305-1317
The Synaptic Basis of GABAA,slow
Matthew I.
Banks1,
Tong-Bin
Li2 and
Robert A.
Pearce1, 2, 3
Departments of 1 Anesthesiology and
2 Anatomy, and 3 Neuroscience Training Program,
University of Wisconsin, Madison, Wisconsin 53706
Although two kinetically distinct evoked GABAA
responses (GABAA,fast and GABAA,slow)
have been observed in CA1 pyramidal neurons, studies of spontaneous
IPSCs (sIPSCs) in these neurons have reported only a single population
of events that resemble GABAA,fast in their rise and decay
kinetics. The absence of slow sIPSCs calls into question the synaptic
basis of GABAA,slow. We present evidence here that both
evoked responses are synaptic in origin, because two classes of
minimally evoked, spontaneous and miniature IPSCs exist that correspond
to GABAA,fast and GABAA,slow. Slow sIPSCs occur
infrequently, suggesting that the cells underlying these events have a
low spontaneous firing rate, unlike the cells giving rise to fast
sIPSCs. Like evoked GABAA,fast and
GABAA,slow, fast and slow sIPSCs are modulated
differentially by furosemide, a subtype-specific GABAA
antagonist. Furosemide blocks fast IPSCs by acting directly on the
postsynaptic receptors, because it reduces the amplitude of both
miniature IPSCs and the responses of excised patches to applied GABA.
Thus, in the hippocampus, parallel inhibitory circuits are composed of
separate populations of interneurons that contact anatomically
segregated and pharmacologically distinct postsynaptic receptors.
Key words:
hippocampus; GABAA receptors; furosemide; IPSC; voltage clamp; pyramidal cell
Copyright © 1998 Society for Neuroscience 0270-6474/98/1841305-13$05.00/0
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