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. 2024 Feb 7;20:17448069241230258. doi: 10.1177/17448069241230258

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© The Author(s) 2024

This article is distributed under the terms of the Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 1. — Contributions of the GluN2A and GluN2B Subunits to the induction of LTP in the ACC (a) LTP induced by the pairing training was partially depressed by 0.1 μM (n = 7) or 0.4 μM (n = 9) NVP-AAM077. (b) LTP was partially depressed by 0.3 μM (n = 9) or 3 μM (n = 5) Ro25-6981. (c) LTP was partially depressed by 3 μM ifenprodil (n = 7). (d) The coapplication of 0.4 μM NVP-AAM077 and 0.3 μM Ro25-6981 completely blocked LTP (n = 6). (a)–(d) The insets show averages of six EPSCs 5 min before and 25 min after the pairing training (arrow). The dashed line indicates the basal synaptic responses. (e) Summary of the effects of NMDA receptor subunit antagonists or postsynaptic injection of BAPTA on LTP. *p < .05 compared to baseline. (Adapted from Zhao et al.,¹⁵).