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. 2017 May 18;10:16. doi: 10.1186/s13041-017-0297-8

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 3 — KA receptors mediate the induction of pre-LTP. a Upper panel: In GluK1-/- mice, sample traces of eEPSCs with paired-pulse stimulation at 50 ms during baseline (1) and 60 min after the induction stimulus (2) at a holding membrane potential of -60 mV. Middle panel: GluK2-/-mice showed normal pre-LTP (black circle). GluK1-/- mice showed greatly reduced pre-LTP (red circle. Bottom panel: PPR for the GluK2-/- (black) and GluK1-/-(red) groups. b A specific GluK1 antagonist, UBP310 (10 μM), completely blocked pre-LTP. c Upper panel: A GluK1 agonist, ATPA (1 μM for 10 min), induced long lasting potentiation, recorded for 2 h. Bottom panel: Averaged data of PPR change before and after ATPA application. d Summary of the effects of GluK2-/-, GluK1-/-, a GluK1 antagonist or a GluK1 agonist on pre-LTP. The amplitudes of eEPSCs in GluK1-/- or UBP310 groups were significantly decreased compared with control pre-LTP. There was no difference among control pre-LTP, GluK2-/- and ATPA. Modified from Koga et al [38]