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This study (Q25) is one of a series of studies performed in the Szechtman lab at McMaster University and deposited in the FRDR public repository as a collection under the name "A Digital Library of Behavioural Performance in Standardized Conditions - Szechtman Lab Collection". This collection as a whole constitutes a big dataset containing raw data objects of video, track, and path plot records of rats exploring for 55 minutes a large testing environment in a standardized paradigm during chronic treatment with psychostimulant drugs; for details of this big dataset see, https://www.frdr-dfdr.ca/repo/collection/szechtmanlab. The historical context for study Q25 was Project_01 entitled: "Probing the neural circuit mediating sensitization and compulsive checking". This project had two separate studies, designated as Q25Bla1 and Q25Bla2. The title of study Q25Bla1 was "Probing the neural circuit mediating sensitization and compulsive checking: role of the basal lateral amygdala (BLA) on development" and the title of study Q25Bla2 was "Probing the neural circuit mediating sensitization and compulsive checking: role of the basal lateral amygdala (BLA) on expression". Title of experiment in Q25Bla1 was "Effect of an NMDA lesion of the BLA on the development of sensitization and compulsive checking" and title of experiment in Q25Bla2 was "Effect of an NMDA lesion of the BLA on the expression of sensitization and compulsive checking". For the development study (Q25Bla1), rats received a lesion targeted at the BLA and the effect of this lesion on the induction of compulsive checking in our standard paradigm was measured. For the expression study (Q25Bla2), rats received our standard treatment to induce compulsive checking and then received a lesion targeted at the BLA and the effect of this lesion on the expression of compulsive checking was measured. This dataset has the same Design and Procedure as dataset deposits for StudyID Q26 doi:10.20383/102.0438 and StudyID Q28 doi:10.20383/102.0436

Background: Cannabinoids induce biphasic effects on memory depending on stress levels. We previously demonstrated that different stress intensities, experienced soon after encoding, impaired rat short-term recognition memory in a time-of-day-dependent manner, and that boosting endocannabinoid anandamide (AEA) levels restored memory performance. Here, we examined if two different stress intensities and time-of-day alter hippocampal endocannabinoid tone, and whether these changes modulate short-term memory. Methods: Male Sprague-Dawley rats were subjected to an object recognition task and exposed, at two different times of the day (i.e., morning or afternoon), to low or high stress conditions, immediately after encoding. Memory retention was assessed 1 hr later. Hippocampal AEA and 2-arachidonoyl glycerol (2-AG) content and the activity of their primary degrading enzymes, fatty acid amide hydrolase (FAAH) and monoacylglycerol lipase (MAGL), were measured soon after testing. Results: Consistent with our previous findings, low stress impaired 1-hr memory performance only in the morning, whereas exposure to high stress impaired memory independently of testing time. Stress exposure decreased AEA levels independently of memory alterations. Interestingly, exposure to high stress decreased 2-AG content and, accordingly, increased MAGL activity, selectively in the afternoon. Thus, to further evaluate 2-AG's role in the modulation of short-term recognition memory, rats were given bilateral intra-hippocampal injections of the 2-AG hydrolysis inhibitor KML29 immediately after training, then subjected to low or high stress conditions and tested 1 hr later. Conclusions: KML29 abolished the time-of-day-dependent impairing effects of stress on short-term memory, ameliorating short-term recognition memory performance.