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. 2017 Jul 26;7(7):170032. doi: 10.1098/rsob.170032

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© 2017 The Authors.

Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.

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Figure 5. — Involvement of endogenous NMDA receptor ligand(s) in activity-dependent decline of I_Ca. I_Ca were elicited by a train of 30 square depolarizing pulses (to 0 mV, duration: 1 ms). Sample records show the first (1st) and 26th–30th averaged I_Ca (ss, superimposed), which are normalized to the first I_Ca, in the absence (left traces) or presence (right traces) of d-AP5 (500 µM). Data points and bars represent mean ± s.e.m. of the normalized I_Ca amplitude in the presence (filled circles) or absence (open circles) of d-AP5 in the aCSF. (a) Activity-dependent decline of I_Ca amplitude by 20 Hz stimuli. No significant difference. (b) Activity-dependent facilitation of I_Ca amplitude by 200 Hz stimuli. No significant difference. (c) Activity-dependent decline of I_Ca amplitude by 20 Hz stimuli in the presence of the glutamate transporter inhibitor TBOA (100 µM). In the presence of d-AP5, I_Ca decline became significantly less (p < 0.05, Student's paired t-test). A horizontal scale bar in the superimposed sample traces indicates 1 ms.