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Hyperpolarizing synaptic potentials evoked in CA1 pyramidal cells by glutamate stimulation of interneurons from the oriens/alveus border of rat hippocampal slices. II. sensitivity to GABA antagonists

Hyperpolarizing synaptic potentials evoked in CA1 pyramidal cells by glutamate stimulation of... The receptor type mediating the inhibitory postsynaptic potentials (glut‐IPSPs), recorded in CA1 pyramidal cells, as a result of glutamate stimulation of interneurons in stratum oriens near the alveus (O/A) was assessed and compared to the type mediating recurrent IPSPs evoked by recurrent activation of interneurons through glutamate stimulation of pyramidal cells in stratum pyramidale (PYR). In response to repetitive electrical stimulation, the peak amplitude of both the O/A glut‐IPSP and the PYR glut‐IPSP was attenuated (n = 5) in parallel to the reduction in amplitude of the early and late components of the electrically evoked response (stimulus‐evoked disinhibition). This suggested the involvement of GABAergic receptors and attested that the interneurons activated during glut‐IPSPs were also involved in the circuitry of the electrically evoked IPSPs. The local application of the selective GABAA antagonist bicuculline (100–200 μM) to the slice resulted in a significant reduction in the amplitude of both the O/A (by 76.5%; n = 9) and PYR (by 86.2%; n = 5) glut‐IPSPs, in parallel to a decrease of the electrically evoked early IPSP, but not of the late IPSP. The presence of the GABAB antagonist 2‐hydroxy‐saclofen (1 mM) was able to significantly reduce the amplitude of the O/A glut‐IPSPs (by 27.5%; n = 7) and of the electrically evoked late IPSP, but not the PYR glut‐IPSP (n = 3). Although the application of phaclofen (20 mM) to the slice reduced the amplitude of the O/A glut‐IPSPs (n = 3), the reduction was not statistically significant. These results suggest that recurrent IPSPs elicited from activation of interneurons by stimulation of pyramidal cells are mediated solely via GABAA receptors. Inhibitory postsynaptic potentials elicited from stimulation of interneurons in O/A were also mediated mostly by GABAA receptors, but in addition, displayed a minor component mediated by GABAB receptors. Therefore, since a large proportion of interneurons in O/A are recurrently excited by pyramidal cells (Lacaille J‐C et al., 1987, J Neurosci 7:1979–1993), and since recurrent IPSPs appeared mediated by GABAA receptors, a subpopulation of interneurons activated from O/A might exist that do not receive recurrent excitation but can inhibit pyramidal cells via GABAB receptors. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hippocampus Wiley

Hyperpolarizing synaptic potentials evoked in CA1 pyramidal cells by glutamate stimulation of interneurons from the oriens/alveus border of rat hippocampal slices. II. sensitivity to GABA antagonists

Samulack, Donald D.; Lacaille, Jean‐Claude
Hippocampus , Volume 3 (3) – Jan 1, 1993
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References (35)

Publisher
Wiley
Copyright
Copyright © 1993 Wiley Subscription Services
ISSN
1050-9631
eISSN
1098-1063
DOI
10.1002/hipo.450030309
pmid
8102583
Publisher site
See Article on Publisher Site

Abstract

The receptor type mediating the inhibitory postsynaptic potentials (glut‐IPSPs), recorded in CA1 pyramidal cells, as a result of glutamate stimulation of interneurons in stratum oriens near the alveus (O/A) was assessed and compared to the type mediating recurrent IPSPs evoked by recurrent activation of interneurons through glutamate stimulation of pyramidal cells in stratum pyramidale (PYR). In response to repetitive electrical stimulation, the peak amplitude of both the O/A glut‐IPSP and the PYR glut‐IPSP was attenuated (n = 5) in parallel to the reduction in amplitude of the early and late components of the electrically evoked response (stimulus‐evoked disinhibition). This suggested the involvement of GABAergic receptors and attested that the interneurons activated during glut‐IPSPs were also involved in the circuitry of the electrically evoked IPSPs. The local application of the selective GABAA antagonist bicuculline (100–200 μM) to the slice resulted in a significant reduction in the amplitude of both the O/A (by 76.5%; n = 9) and PYR (by 86.2%; n = 5) glut‐IPSPs, in parallel to a decrease of the electrically evoked early IPSP, but not of the late IPSP. The presence of the GABAB antagonist 2‐hydroxy‐saclofen (1 mM) was able to significantly reduce the amplitude of the O/A glut‐IPSPs (by 27.5%; n = 7) and of the electrically evoked late IPSP, but not the PYR glut‐IPSP (n = 3). Although the application of phaclofen (20 mM) to the slice reduced the amplitude of the O/A glut‐IPSPs (n = 3), the reduction was not statistically significant. These results suggest that recurrent IPSPs elicited from activation of interneurons by stimulation of pyramidal cells are mediated solely via GABAA receptors. Inhibitory postsynaptic potentials elicited from stimulation of interneurons in O/A were also mediated mostly by GABAA receptors, but in addition, displayed a minor component mediated by GABAB receptors. Therefore, since a large proportion of interneurons in O/A are recurrently excited by pyramidal cells (Lacaille J‐C et al., 1987, J Neurosci 7:1979–1993), and since recurrent IPSPs appeared mediated by GABAA receptors, a subpopulation of interneurons activated from O/A might exist that do not receive recurrent excitation but can inhibit pyramidal cells via GABAB receptors.

Journal

Hippocampus – Wiley

Published: Jan 1, 1993

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