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The Journal of Neuroscience, February 15, 1998, 18(4):1305-1317

The Synaptic Basis of GABA_A,slow

Matthew I. Banks¹, Tong-Bin Li² and Robert A. Pearce^{1, 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 GABA_A responses (GABA_A,fast and GABA_A,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 GABA_A,fast in their rise and decay kinetics. The absence of slow sIPSCs calls into question the synaptic basis of GABA_A,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 GABA_A,fast and GABA_A,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 GABA_A,fast and GABA_A,slow, fast and slow sIPSCs are modulated differentially by furosemide, a subtype-specific GABA_A 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; GABA_A receptors; furosemide; IPSC; voltage clamp; pyramidal cell

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Copyright © 1998 Society for Neuroscience  0270-6474/98/1841305-13$05.00/0

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