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Theta is one of the most prominent extracellular synchronous oscillations in the mammalian brain. Hippocampal theta relies on an intact medial septum (MS) and has been consistently recorded during the training phase of some learning paradigms, suggesting that it may be implicated in hippocampus-dependent long-term memory processing. Object recognition memory (ORM) allows animals to identify familiar items and is essential for remembering facts and events. In rodents, long-term ORM formation requires a functional hippocampus but the involvement of the MS in this process remains controversial. We found that training adult male Wistar rats in a long-term ORM-inducing learning task involving exposure to two different, but behaviorally equivalent novel stimuli objects increased hippocampal theta power, and that suppressing theta via optogenetic MS inactivation caused amnesia. Importantly, the amnesia was specific to the object the animals were exploring when the MS was inactivated. Taken together, our results indicate that the MS is necessary for long-term ORM formation and suggest that hippocampal theta activity is causally linked to this process. [ABSTRACT FROM AUTHOR]

Avoidance memory is destabilized when recalled concurrently with conflicting information, and must undergo a hippocampus-dependent restabilization process called reconsolidation to persist. CaMKII is a serine/threonine protein kinase essential for memory processing; however, its possible involvement in avoidance memory reconsolidation has not yet been studied. Using pharmacological, electrophysiological and optogenetic tools, we found that in adult male Wistar rats hippocampal CaMKII is necessary to reconsolidate avoidance memory, but not to keep it stored while inactive, and that blocking reconsolidation via CaMKII inhibition erases learned avoidance responses. [ABSTRACT FROM AUTHOR]

Object recognition memory (ORM) allows identification of previously encountered items and is therefore crucial for remembering episodic information. In rodents, reactivation during recall in the presence of a novel object destabilizes ORM and initiates a Zif268 and protein synthesis-dependent reconsolidation process in the hippocampus that links the memory of this object to the reactivated recognition trace. Hippocampal NMDA receptors (NMDARs) modulate Zif268 expression and protein synthesis and regulate memory stability but their possible involvement in the ORM destabilization/reconsolidation cycle has yet to be analyzed in detail. We found that, in adult male Wistar rats, intra dorsal-CA1 administration of the non-subunit selective NMDAR antagonist AP5, or of the GluN2A subunit-containing NMDAR antagonist TCN201, 5 min after an ORM reactivation session in the presence of a novel object carried out 24 h post-training impaired retention 24 h later. In contrast, pre-reactivation administration of the GluN2B subunit-containing NMDAR antagonist RO25–6981 had no effect on ORM recall or retention but impeded the amnesia caused by Zif268 silencing and protein synthesis inhibition in dorsal CA1. Our results indicate that GluN2B-containing hippocampal NMDARs are necessary for ORM destabilization whereas GluN2A-containing NMDARs are involved in ORM reconsolidation, and suggest that modulation of the relative activity of these receptor subtypes during recall regulates ORM persistence. [ABSTRACT FROM AUTHOR]

Object recognition memory (ORM) serves to distinguish familiar items from novel ones. Reconsolidation is the process by which active memories are updated. The hippocampus is engaged in ORM reconsolidation through a mechanism involving induction of long-term potentiation (LTP). The transcription factor Zif268 is essential for hippocampal LTP maintenance and has been frequently associated with memory processes. However, its possible involvement in ORM reconsolidation has not been determined conclusively. Using Zif268 antisense oligonucleotides in combination with behavioural, biochemical and electrophysiological tools in rats, we found that hippocampal Zif268 is necessary to update ORM through reconsolidation but not to retrieve it or keep it stored. Our results also suggest that knocking down hippocampal Zif268 during ORM reconsolidation deletes the active recognition memory trace. [ABSTRACT FROM AUTHOR]

Often, retrieval cues are not uniquely related to one specific memory, which could lead to memory interference. Controlling interference is particularly important during episodic memory retrieval or when remembering specific events in a spatiotemporal context. Despite a clear involvement of prefrontal cortex (PFC) in episodic memory in human studies, information regarding the mechanisms and neurotransmitter systems in PFC involved in memory is scarce. Although the serotoninergic system has been linked to PFC functionality and modulation, its role inmemoryprocessing is poorly understood. We hypothesized that the serotoninergic system in PFC, in particular the 5-HT2A receptor (5-HT2AR) could have a role in the control of memory retrieval. In this work we used different versions of the object recognition task in rats to study the role of the serotoninergic modulation in the medial PFC (mPFC) in memory retrieval. We found that blockade of 5-HT2AR in mPFC affects retrieval of an object in context memory in a spontaneous novelty preference task, while sparing single-item recognition memory. We also determined that 5-HT2ARs in mPFC are required for hippocampal-mPFC interaction during retrieval of this type of memory, suggesting that the mPFC controls the expression of memory traces stored in the hippocampus biasing retrieval to the most relevant one. [ABSTRACT FROM AUTHOR]