The retrosplenial cortex (RSC) is implicated on navigation and contextual memory. Lesions studies showed that the RSC shares functional similarities with the hippocampus (HP). Here we evaluated the role of the anterior RSc (aRSc) in the "what" and "where" components of recognition memory and contrasted it with that of the dorsal HP (dHP). Our behavioral and molecular findings show functional differences between the aRSC and the dHP in recognition memory. The inactivation of the aRSC, but not the dHP, impairs the consolidation and expression of the "what" memory component. In addition, object recognition task is accompanied by c-Fos levels increase in the aRSC. Interestingly, we found that the aRSC is recruited to process the "what" memory component only if it is active during acquisition. In contrast, both the aRSC and dHP are required for encoding the "where" component, which correlates with c-Fos levels increase. Our findings introduce a novel role of the aRSC in recognition memory, processing not only the "where", but also the "what" memory component. open Scientific RepoRtS | (2020) 10:4002 | https://doi.org/10.1038/s41598-020-60937-zwww.nature.com/scientificreports www.nature.com/scientificreports/ functions of the aRSC from those of the dHP, given that the last one is only required for the "where" component of recognition memory. ResultsaRSC, but not dHP, is required for the "what" memory component processing. To make a comparative study about the participation of aRSC and dHP in the "what" component of the recognition memory, we decided to study object recognition memory in the non-spatial Y-maze (Y-OR) task 28 . Due to the high walls, small corridors and the lack of explicit clues in the Y-maze, the Y-OR task has minimal spatial information and therefore a negligible "where" component. First, we validated the Y-OR task by transient inactivation of the PRh, confirming its requirement for object recognition memory ( Supplementary Fig. S1; p = 0.0031, t = 3.774, df = 11; Muscimol vs. Vehicle, Student's t test, n = 5-7). Then, we analyzed the participation of the aRSC and dHP in the formation of Y-OR long-term memory (LTM) by infusing the GABA A receptor agonist muscimol (0.1 μg/μl) or vehicle (saline) into the aRSC or the dHP immediately after the sample phase (training session), and we evaluated memory expression 24 h later during the choice phase (Fig. 1a). We found memory impairment associated to the Scientific RepoRtS | (2020) 10:4002 | https://doi.empty maze during 15 min for 2 days. Exposition time during sample and choice phases were the same as the Y-OR, with the difference that in this task the objects were located facing each other in the middle of the maze ( Supplementary Fig. S6B). Object Location. OL task was performed in the same apparatus that the SOR. This task was adapted fromEnnaceur and collaborators 37 . The habituation session consisted in letting the rat explore the empty apparatus during 20 min for 3 days. During the sample phase two identical objects were presented to the rat, each on...

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Understanding how stored information emerges is a main question in the neurobiology of memory that is now increasingly gaining attention. However, molecular events underlying this memory stage, including involvement of protein synthesis, are not well defined. Mammalian target of rapamycin complex 1 (mTORC1), a central regulator of protein synthesis, has been implicated in synaptic plasticity and is required for memory formation. Using inhibitory avoidance (IA), we evaluated the role of mTORC1 in memory retrieval. Infusion of a selective mTORC1 inhibitor, rapamycin, into the dorsal hippocampus 15 or 40 min but not 3 h before testing at 24 h reversibly disrupted memory expression even in animals that had already expressed IA memory. Emetine, a general protein synthesis inhibitor, provoked a similar impairment. mTORC1 inhibition did not interfere with short-term memory retrieval. When infused before test at 7 or 14 but not at 28 days after training, rapamycin impaired memory expression. mTORC1 blockade in retrosplenial cortex, another structure required for IA memory, also impaired memory retention. In addition, pretest intrahippocampal rapamycin infusion impaired object location memory retrieval. Our results support the idea that ongoing protein synthesis mediated by activation of mTORC1 pathway is necessary for long but not for short term memory.