LTP in cortical input also depends on presynaptic KAR.

<p><b>A</b>-<b>C</b>, Graphs summarizing LTP experiments showing the effect of Ca²⁺ chelators (<b>A</b>: BAPTA, BAPTA-AM), metabotropic glutamate receptor antagonist (<b>B</b>: MCPG) and selective KAR antagonists (<b>C</b>: UBP296, ACET) on the induction of LTP in cortical input. The respective insets show superimposition of averaged EPSCs recorded before and after the induction in the presence of each drug. Scale bars (<b>A</b>-<b>C</b>) 50 pA, 20 ms. <b>D</b>, Quantification of pharmacological analysis (<b>A</b>-<b>C</b>). Control was obtained from the result in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0074668#pone-0074668-g001" target="_blank">Figure 1E</a>. LTP in cortical input was blocked by BAPTA-AM (97 ± 15% of baseline, n=8, unpaired <i>t</i> test, p<0.01 versus control), but not by BAPTA (179 ± 27% of baseline, n=6, unpaired <i>t</i> test, p=0.53 versus control). This potetiation was resistant to MCPG (170 ± 18% of baseline, n=6, unpaired <i>t</i> test, p=0.68 versus control), but it was prevented by either UBP296 (105 ± 7% of baseline, n=5, unpaired <i>t</i> test, p<0.01 versus control) or ACET (88 ± 5% of baseline, n=5, unpaired <i>t</i> test, p<0.01 versus control). **p<0.01.