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. 2021 Aug 7;24(11):907–919. doi: 10.1093/ijnp/pyab055

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© The Author(s) 2021. Published by Oxford University Press on behalf of CINP.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — AICP treatment immediately after fear extinction increases synaptic α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors. (A) Confocal images from basolateral amygdala (BLA) of vehicle-extinction (top) and AICP extinction (100 ng/side, i-BLA, bottom) WT mice immunostained for AMPA receptor GluA1 subunit and PSD 95. Arrowheads showing colocalized puncta. (B) Quantification of immunostaining; AICP treatment led to a significant increase in total GluA1 puncta (P = .0196). Trend for an increase in PSD 95 immunoreactive puncta in AICP-extinction group (P = .0926). Significant increase in total GluA1-PSD 95 colocalized puncta in AICP-extinction group (P = .0002). (C) Confocal images from BLA of vehicle-extinction (top) and AICP-extinction (bottom) WT mice immunostained for bassoon, GluA1 and PSD 95. Arrowheads show colocalized puncta. (D) Quantification of immunostaining. No significant change in bassoon-PSD 95 colocalized puncta by AICP (P = .1387). Significant increase in bassoon/GluA1/PSD 95 colocalized puncta (P = .0282) by AICP treatment. Bar graphs represent mean ± SEM, each data point representing 22–24 images from n = 3 vehicle and n = 5 AICP mice. Data were analyzed by unpaired t test.