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Heterosynaptic enhancement of the excitability of hippocampal mossy fibers by long‐range spill‐over of glutamate
Author(s) -
Uchida Takeshi,
Fukuda Satoshi,
Kamiya Haruyuki
Publication year - 2012
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20885
Subject(s) - kainate receptor , neuroscience , chemistry , mossy fiber (hippocampus) , glutamate receptor , long term depression , gabaa receptor , nmda receptor , biophysics , ampa receptor , hippocampal formation , receptor , biology , biochemistry , dentate gyrus
Several classes of ionotropic receptors have been reported to depolarize the axonal membrane of hippocampal mossy fibers. Both kainate receptors and GABA A receptors are localized on axons and/or presynaptic terminals, and these receptors have been known to be activated by synaptically released glutamate and GABA which spill out from the synaptic clefts. However the relative contribution of these two receptors in modulating the excitability of mossy fiber axon was not reported so far. In this study, we revealed that glutamate spilled out from commissural/associational synapses evoked the facilitation of antidromic population spikes of mossy fibers. Increase in amplitude and decrease in latency of population spikes suggest that the number of recruited mossy fibers increases by depolarization of axonal membrane. Application of non‐NMDA receptor antagonist CNQX (10 μM) almost abolished this effect. TBOA (30 μM), an inhibitor of glutamate transporter, prolonged the duration of heterosynaptic facilitation. These results suggest that glutamate released from distant commissural/associational synapses spills out from synaptic cleft and activates the kainate receptors on the mossy fibers of CA3 region, and plays a major role in modulating presynaptic excitability than GABA. © 2010 Wiley Periodicals, Inc.

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