Kainate receptor‐mediated presynaptic inhibition at the mouse hippocampal mossy fibre synapse

Kainate receptor‐mediated presynaptic inhibition at the mouse hippocampal mossy fibre synapse 1 The presynaptic action of kainate (KA) receptor activation at the mossy fibre‐CA3 synapse was examined using fluorescence measurement of presynaptic Ca2+ influx as well as electrophysiological recordings in mouse hippocampal slices. 2 Bath application of a low concentration (0·2 μM) of KA reversibly increased the amplitude of presynaptic volley evoked by stimulation of mossy fibres to 146 ± 6 % of control (n= 6), whereas it reduced the field excitatory postsynaptic potential (EPSPs) to 30 ± 4 %. 3 The potentiating effect of KA on the presynaptic volleys was also observed in Ca2+‐free solution, and was partly antagonized by (2S,4R)‐4‐methylglutamic acid (SYM 2081, 1 μM), which selectively desensitizes KA receptors. 4 The antidromic population spike of dentate granule cells evoked by stimulation of mossy fibres was increased by application of 0·2 μM KA to 160 ± 10 % of control (n= 6). Whole‐cell current‐clamp recordings revealed that the stimulus threshold for generating antidromic spikes recorded from a single granule cell was lowered by KA application. 5 Application of KA (0·2 μM) suppressed presynaptic Ca2+ influx to 78 ± 4 % of control (n= 6), whereas the amplitude of the presynaptic volley was increased. 6 KA at 0·2 μM reversibly suppressed excitatory postsynaptic currents (EPSCs) evoked by mossy fibre simulation to 38 ± 9 % of control (n= 5). 7 These results suggest that KA receptor activation enhances the excitability of mossy fibres, probably via axonal depolarization, and reduces action potential‐induced Ca2+ influx, thereby inhibiting mossy fibre EPSCs presynaptically. This novel presynaptic inhibitory action of KA at the mossy fibre‐CA3 synapse may regulate the excitability of highly interconnected CA3 networks. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

Kainate receptor‐mediated presynaptic inhibition at the mouse hippocampal mossy fibre synapse

The Journal of Physiology, Volume 523 (3) – Mar 1, 2000

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Publisher
Wiley
Copyright
Copyright © 2000 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0022-3751
eISSN
1469-7793
DOI
10.1111/j.1469-7793.2000.t01-1-00653.x
Publisher site
See Article on Publisher Site

Abstract

1 The presynaptic action of kainate (KA) receptor activation at the mossy fibre‐CA3 synapse was examined using fluorescence measurement of presynaptic Ca2+ influx as well as electrophysiological recordings in mouse hippocampal slices. 2 Bath application of a low concentration (0·2 μM) of KA reversibly increased the amplitude of presynaptic volley evoked by stimulation of mossy fibres to 146 ± 6 % of control (n= 6), whereas it reduced the field excitatory postsynaptic potential (EPSPs) to 30 ± 4 %. 3 The potentiating effect of KA on the presynaptic volleys was also observed in Ca2+‐free solution, and was partly antagonized by (2S,4R)‐4‐methylglutamic acid (SYM 2081, 1 μM), which selectively desensitizes KA receptors. 4 The antidromic population spike of dentate granule cells evoked by stimulation of mossy fibres was increased by application of 0·2 μM KA to 160 ± 10 % of control (n= 6). Whole‐cell current‐clamp recordings revealed that the stimulus threshold for generating antidromic spikes recorded from a single granule cell was lowered by KA application. 5 Application of KA (0·2 μM) suppressed presynaptic Ca2+ influx to 78 ± 4 % of control (n= 6), whereas the amplitude of the presynaptic volley was increased. 6 KA at 0·2 μM reversibly suppressed excitatory postsynaptic currents (EPSCs) evoked by mossy fibre simulation to 38 ± 9 % of control (n= 5). 7 These results suggest that KA receptor activation enhances the excitability of mossy fibres, probably via axonal depolarization, and reduces action potential‐induced Ca2+ influx, thereby inhibiting mossy fibre EPSCs presynaptically. This novel presynaptic inhibitory action of KA at the mossy fibre‐CA3 synapse may regulate the excitability of highly interconnected CA3 networks.

Journal

The Journal of PhysiologyWiley

Published: Mar 1, 2000

References

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