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Heterogeneity in presynaptic regulation of GABA release from hippocampal inhibitory neurons

*Corresponding author for this work
  • Duke University
Scholary Output:
Contribution to journal
Article
Peer-review

Abstract

Release of GABA from the terminals of hippocampal inhibitory neurons is inhibited by activation of GABAB autoreceptors and μ opioid receptors. However, it is not known whether these presynaptic processes affect all inhibitory synapses equally. We examined the effects of the GABAB receptor agonist baclofen and the p opioid receptor agonist DAGO on postsynaptic currents evoked by minimal stimulation of inhibitory fibers (mePSCs) in area CA3. Baclofen reversibly depressed approximately half of the meIPSCs evoked in the stratum pyramidale. The remaining meIPSCs were unaffected despite a coincident depression of spontaneous IPSCs. In contrast, all meIPSCs were depressed by DAGO. In addition, minimal stimulation in the stratum radiatum evoked me1PSCs that were always depressed by baclofen. These results indicate that regulation of GABA release by GABAB autoreceptors occurs at a subset of inhibitory synapses and that GABAB-resistant inhibitory synapses are located on pyramidal neuron somata. Hippocampal inhibitory neurons may be heterogeneous with respect to presynaptic receptor-mediated regulation of GABA release.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 1057-1067 (11 pages)

Journal (Volume, Issue Number)

Neuron (Volume 11, Issue 6)

Publication milestones

  • Published - 12/1993

Publication status

Published - 12/1993

ISSN

0896-6273

Publication IDs

  • Scopus: 0027729948
  • PubMed: 8274277

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Scopus
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1
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Funding Details

We thank Dr. Robert Pearce for discussion of unpublished results, Dr. David Mott for his helpful comments on the manuscript, and M. I. Tayyeb and D. S. Barr for expert technical assistance. We also thank Drs. S. J. Mickel and H.-R. Olpe, Ciba-Geigy, Basel, for providing CGP 55845A, and Astra Pharmaceuticals for providing QX-314. This research was supported by National Insti-
FundersFunding number
Vet. Administration Medical Center
-
NINDS
P01NS017771