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Amorphous organic long‐persistent luminescence materials (OLPLMs) can realize simpler solution processing and large‐area uniform luminescence, which luminescent properties are significantly influenced by the rigid environment. However, research on utilizing the rigidity to promote long‐persistent luminescence (LPL) properties of amorphous OLPLMs is still relatively rare due to the lack of an unambiguous and effective strategy to construct the rigid environment. Here, we propose a universal strategy to enhance the LPL performance of organic host‐guest doping systems by UV curing, which utilizes the rigid environment constructed by UV curing to promote the interaction between host and guest, thus inducing the generation of highly efficient LPL performance. This solution‐processable, large‐area and “easy to realize” material fabrication strategy can make amorphous OLPLMs show broader application prospects in some fields, such as anti‐counterfeiting, non‐destructive detection, and pattern marking or indication.This article is protected by copyright. All rights reserved

IntroductionFear memory generalization is regarded as the core characteristic of posttraumatic stress disorder (PTSD) development. However, the mechanism that contributes to the generalization of conditioned fear memory is still unclear. The generalization is generally considered to be a mismatch that occurs during memory consolidation.MethodsFoot shocks and tones were given as unconditioned stress and conditioned stress, respectively for fear conditioning training. Immunofluorescence staining, western blotting and qPCR were performed to determine the expression of different genes in amygdala of mice after fear conditioning training. Cycloheximide was used as a protein synthesis inhibitor and 2-methyl-6-phenylethynyl-pyridine was injected for mGluR5 inhibition.ResultsFear conditioning using caused incremental generalization, which was clearly observed during training. The density of c-Fos+ cells or the synaptic p-NMDAR expression did not differ with stress intensities. Strong-shock fear conditioning could induce significant mGluR5 de novo synthesis in the amygdala, which was not observed in the weak-shock group. Inhibition of mGluR5 impaired fear memory generalization induced by strong-shock fear conditioning, but the generalization level induced by weak-shock training was enhanced.DiscussionThese results indicated that mGluR5 in the amygdala is critical to the function of inappropriate fear memory generalization and suggested that this may be a potential target for the treatment of PTSD.

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