Memory Consolidation Processes Research Articles

Time for considering constraints on procedural memory consolidation processes: Comment on Pan and Rickard (2015) with specific reference to developmental changes.

In the acquisition of some motor skills, sleep may be necessary for the completion of procedural memory consolidation processes, as expressed in delayed "offline" performance gains. Pan and Rickard (2015) conducted an original meta-analysis of the literature on performing an explicitly instructed finger movement sequence and tested the role of sleep versus wake in the enhancement of performance over posttraining delay periods. In this comment we propose that a more-biological, process-oriented framework is needed, allowing for more than a yes-no answer to the question addressed, and suggest methodological issues that may affect the target meta-analysis. We argue that different task demands, task conditions, and developmental differences should be considered a priori rather than expected to emerge from pooled data. For example, several recent studies have indicated that there is a qualitative change in the time course of procedural memory consolidation processes at puberty, between the ages of 12 and 17. Before puberty, consolidation processes are reflected in enhancement of task performance over sleep and wake periods alike. In their extensive set of relevant empirical data the authors included a number of developmental studies comparing children with adults (expecting "child status" effects) but did not fully consider developmental changes. We show that the inclusion of the 6 studies of childhood, comprising 13 groups, biases the meta-analysis toward the conclusion that skill enhancement is similar across wake and sleep periods. (PsycINFO Database Record

Does Sleep Improve Your Grammar? Preferential Consolidation of Arbitrary Components of New Linguistic Knowledge.

We examined the role of sleep-related memory consolidation processes in learning new form-meaning mappings. Specifically, we examined a Complementary Learning Systems account, which implies that sleep-related consolidation should be more beneficial for new hippocampally dependent arbitrary mappings (e.g. new vocabulary items) relative to new systematic mappings (e.g. grammatical regularities), which can be better encoded neocortically. The hypothesis was tested using a novel language with an artificial grammatical gender system. Stem-referent mappings implemented arbitrary aspects of the new language, and determiner/suffix+natural gender mappings implemented systematic aspects (e.g. tib scoiffesh + ballerina, tib mofeem + bride; ked jorool + cowboy, ked heefaff + priest). Importantly, the determiner-gender and the suffix-gender mappings varied in complexity and salience, thus providing a range of opportunities to detect beneficial effects of sleep for this type of mapping. Participants were trained on the new language using a word-picture matching task, and were tested after a 2-hour delay which included sleep or wakefulness. Participants in the sleep group outperformed participants in the wake group on tests assessing memory for the arbitrary aspects of the new mappings (individual vocabulary items), whereas we saw no evidence of a sleep benefit in any of the tests assessing memory for the systematic aspects of the new mappings: Participants in both groups extracted the salient determiner-natural gender mapping, but not the more complex suffix-natural gender mapping. The data support the predictions of the complementary systems account and highlight the importance of the arbitrariness/systematicity dimension in the consolidation process for declarative memories.

Task-dependent role for dorsal striatum metabotropic glutamate receptors in memory.

The effect of post-training intradorsal striatal infusion of metabotropic glutamate receptor (mGluR) drugs on memory consolidation processes in an inhibitory avoidance (IA) task and visible/hidden platform water maze tasks was examined. In the IA task, adult male Long-Evans rats received post-training intracaudate infusions of the broad spectrum mGluR antagonist alpha-methyl-4-carboxyphenylglycine (MCPG; 1.0, 2.0 mM/0.5 microL), the group I/II mGluR agonist 1-aminocyclopentane-1,3-carboxylic acid (ACPD; 0.5 or 1.0 microM/0.5 microL), or saline immediately following footshock training, and retention was tested 24 h later. In the visible- and hidden-platform water maze tasks, rats received post-training intracaudate infusions of ACPD (1.0 microM), MCPG (2.0 mM), or saline immediately following an eight-trial training session, followed by a retention test 24 h later. In the IA task, post-training infusion of ACPD (0.5 and 1.0 microM) or MCPG (1.0 and 2.0 mM) impaired retention. In the IA and visible-platform water maze tasks, post-training infusion of ACPD (1.0 microM), or MCPG (2.0 mM) impaired retention. In contrast, neither drug affected retention when administered post-training in the hidden-platform task, consistent with the hypothesized role of the dorsal striatum in stimulus-response habit formation. When intradorsal striatal injections were delayed 2 h post-training in the visible-platform water maze task, neither drug affected retention, indicating a time-dependent effect of the immediate post-training injections on memory consolidation. It is hypothesized that MCPG impaired memory via a blockade of postsynaptic dorsal striatal mGluR's, while the impairing effect of ACPD may have been caused by an influence of this agonist on presynaptic "autoreceptor" striatal mGluR populations.

Inter-hemispheric connectivity in the fusiform gyrus supports memory consolidation for faces.

This study investigated how changes of functional connectivity over time accompany consolidation of face memories. Based on previous research, it was hypothesized that connectivity changes in networks initially active during face perception and face encoding would be associated with individual recognition memory performance. Resting-state functional connectivity was examined shortly before, shortly after and about 40min after incidental learning of faces. Memory performance was assessed in a surprise recognition test shortly after the last resting-state session. Results reveal that memory performance-related connectivity between the left fusiform face area and other brain areas gradually changed over the course of the experiment. Specifically, the increase in connectivity with the contralateral fusiform gyrus, the hippocampus, the amygdala and the inferior frontal gyrus correlated with recognition memory performance. As the increase in connectivity in the two final resting-state sessions was associated with memory performance, the present results demonstrate that memory formation is not restricted to the incidental learning phase but continues and increases in the following 40min. It is discussed that the delayed increase in inter-hemisphere connectivity between the left and right fusiform gyrus is an indicator for memory formation and consolidation processes.

Neuronal Firing Rate Homeostasis Is Inhibited by Sleep and Promoted by Wake

Homeostatic mechanisms stabilize neural circuit function by keeping firing rates within a set-point range, but whether this process is gated by brain state is unknown. Here, we monitored firing rate homeostasis in individual visual cortical neurons in freely behaving rats as they cycled between sleep and wake states. When neuronal firing rates were perturbed by visual deprivation, they gradually returned to a precise, cell-autonomous set point during periods of active wake, with lengthening of the wake period enhancing firing rate rebound. Unexpectedly, this resetting of neuronal firing was suppressed during sleep. This raises the possibility that memory consolidation or other sleep-dependent processes are vulnerable to interference from homeostatic plasticity mechanisms. PAPERCLIP.

Higher-Order Sensory Cortex Drives Basolateral Amygdala Activity during the Recall of Remote, but Not Recently Learned Fearful Memories.

How and where in the brain do we store the affective/motivational significance of sensory stimuli acquired through life experiences? Scientists have long investigated how "limbic" structures, such as the amygdala, process affective stimuli. Here we show that retrieval of well-established threat memories requires the functional interplay between higher-order components of the auditory cortex and the amygdala via synchrony in the theta range. This functional connectivity is a result of memory consolidation processes and is characterized by a predominant cortical to amygdala direction of information transfer. This connectivity is predictive of the animals' ability to recognize auditory stimuli as aversive. In the absence of this necessary cortical activity, the amygdala is unable to distinguish between frightening and neutral stimuli.

The consolidation of a motor skill in young adults with ADHD: Shorter practice can be better

Practice on a given sequence of movements can lead to robust procedural memory (skill). In young adults, in addition to gains in performance accrued during practice, speed and accuracy can further improve overnight; the latter, delayed, ‘offline’, gains are thought to emerge when procedural memory consolidation processes are completed. A recent study suggested that female college students with ADHD show an atypical procedural memory consolidation phase, specifically, gaining speed but losing accuracy, overnight. Here, to test if this accuracy loss reflected a cost of overlong training in adults with ADHD, we compared the performance of female college students with (N=16) and without (N=16) ADHD, both groups given a shorter training protocol (80 rather than the standard 160 task repetitions). Speed and accuracy were recorded before training, immediately after, and at 24-h and 2 weeks post-training. The shortened practice session resulted in as robust within-session gains and additional overnight gains in speed at no costs in accuracy, in both groups. Moreover, individuals with ADHD showed as robust speed gains and retention as in the longer training session, but the costs in accuracy incurred in the latter were eliminated. The shortening of practice sessions may benefit motor skill acquisition in ADHD.

Involvement of Dopamine D1/D5 and D2 Receptors in Context-Dependent Extinction Learning and Memory Reinstatement.

Dopamine contributes to the regulation of higher order information processing and executive control. It is important for memory consolidation processes, and for the adaptation of learned responses based on experience. In line with this, under aversive learning conditions, application of dopamine receptor antagonists prior to extinction result in enhanced memory reinstatement. Here, we investigated the contribution of the dopaminergic system to extinction and memory reinstatement (renewal) of an appetitive spatial learning task in rodents. Rats were trained for 3 days in a T-maze (context “A”) to associate a goal arm with a food reward, despite low reward probability (acquisition phase). On day 4, extinction learning (unrewarded) occurred, that was reinforced by a context change (“B”). On day 5, re-exposure to the (unrewarded) “A” context took place (renewal of context “A”, followed by extinction of context “A”). In control animals, significant extinction occurred on day 4, that was followed by an initial memory reinstatement (renewal) on day 5, that was, in turn, succeeded by extinction of renewal. Intracerebral treatment with a D1/D5-receptor antagonist prior to the extinction trials, elicited a potent enhancement of extinction in context “B”. By contrast, a D1/D5-agonist impaired renewal in context “A”. Extinction in the “A” context on day 5 was unaffected by the D1/D5-ligands. Treatment with a D2-receptor antagonist prior to extinction had no overall effect on extinction in context “B” or renewal in context “A”, although extinction of the renewal effect was impaired on day 5, compared to controls. Taken together, these data suggest that dopamine acting on the D1/D5-receptor modulates both acquisition and consolidation of context-dependent extinction. By contrast, the D2-receptor may contribute to context-independent aspects of this kind of extinction learning.

Role of epigenetic modulation in hypobaric hypoxia induced memory impairment

Event Abstract Back to Event Role of epigenetic modulation in hypobaric hypoxia induced memory impairment Rahul Kumar1, Vishal Jain2, Neetu Kushwah1, Aastha Dheer1, Dipti Prasad1 and Shashi B. Singh1* 1 Defense Institute of Physiology and Allied Sciences (DIPAS) DRDO, Neurobiology Department, India 2 Defense Institute of Physiology and Allied Sciences (DIPAS) DRDO, Neurophysiology Department, India Long term memory formation requires a series of cellular as well as molecular adaptation that control the gene expression at the transcription level. However, epigenetic mechanisms such as histone acetylation, methylation, phosphorylation and DNA methylation have emerge critical regulators of transcription during memory consolidation process. Epigenetic mechanism controls gene expression bidirectional i.e. either enhance or repress gene expression. In addition, histone acetylation has been the main mechanism of epigenetics and play important role in memory formation as well as reconsolidation. Stressful environmental conditions such as hypobaric hypoxia (HH) leads to change in learning and memory. Present study is designed to explore global as well as specific histone modifications, mainly acetylation in different brain regions during different duration of HH exposure. Sprague Dawley rats (220 to 230 gm) were exposed to different duration of HH i.e. 1, 3, 7 and 14 days in an animal decompression chamber at an altitude of 25,000 feet. After exposure, rats were sacrificed and hippocampus and cortex were isolated. Activity of histone acetylase (HAT), histone deacetylase (HDAC) and DNA methyl transferase (DNMT) was analyzed using kits. Further specific histone acetylation sites i.e. H2BK5Acetylation, H3K9Acetylation and H4K14Acetylation were also studied in different brain regions. Results from the present study revealed the correlation between expressions of HDAC and HIF-1 alpha which further control other hypoxia responsive genes in both the brain regions. Gradual increased expression of HDAC on HH exposure causes repression of learning and memory related genes. In addition, the decline in H2BK5Ac expression may also account for inactivation of transcription of memory responsive gene leading to decline in memory. In brief, it can be concluded that epigenetic modification at histone acetylation sites may account for HH mediated memory impairment. Keywords: Memory, epigenetic, in vivo, histone acetylation, hypobaric hypoxia Conference: 14th Meeting of the Asian-Pacific Society for Neurochemistry, Kuala Lumpur, Malaysia, 27 Aug - 30 Aug, 2016. Presentation Type: Poster Presentation Session Topic: 14th Meeting of the Asian-Pacific Society for Neurochemistry Citation: Kumar R, Jain V, Kushwah N, Dheer A, Prasad D and Singh SB (2016). Role of epigenetic modulation in hypobaric hypoxia induced memory impairment. Conference Abstract: 14th Meeting of the Asian-Pacific Society for Neurochemistry. doi: 10.3389/conf.fncel.2016.36.00191 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 Aug 2016; Published Online: 11 Aug 2016. * Correspondence: Dr. Shashi B Singh, Defense Institute of Physiology and Allied Sciences (DIPAS) DRDO, Neurobiology Department, New Delhi, North Delhi, India, drshashisingh@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Rahul Kumar Vishal Jain Neetu Kushwah Aastha Dheer Dipti Prasad Shashi B Singh Google Rahul Kumar Vishal Jain Neetu Kushwah Aastha Dheer Dipti Prasad Shashi B Singh Google Scholar Rahul Kumar Vishal Jain Neetu Kushwah Aastha Dheer Dipti Prasad Shashi B Singh PubMed Rahul Kumar Vishal Jain Neetu Kushwah Aastha Dheer Dipti Prasad Shashi B Singh Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Sleep, memory, attention and Neurofeedback

Sleep, memory, attention and Neurofeedback

Sleep-dependent memory consolidation and its implications for psychiatry.

Both sleep disturbance and memory impairment are very common in psychiatric disorders. Since sleep has been shown to play a role in the process of transferring newly acquired information into long-term memory, i.e., consolidation, it is important to highlight this link in the context of psychiatric disorders. Along these lines, after providing a brief overview of healthy human sleep, current neurobiological models on sleep-dependent memory consolidation and resultant opportunities to manipulate the memory consolidation process, recent findings on sleep disturbances and sleep-dependent memory consolidation in patients with insomnia, major depression, schizophrenia, and post-traumatic stress disorder are systematically reviewed. Furthermore, possible underlying neuropathologies and their implications on therapeutic strategies are discussed. This review aims at sensitizing the reader for recognizing sleep disturbances as a potential contributor to cognitive deficits in several disorders, a fact which is often overlooked up to date.

Physical exercise prevents short and long-term deficits on aversive and recognition memory and attenuates brain oxidative damage induced by maternal deprivation

It is known from previous research that physical exercise prevents long-term memory deficits induced by maternal deprivation in rats. But we could not assume similar effects of physical exercise on short-term memory, as short- and long-term memories are known to result from some different memory consolidation processes. Here we demonstrated that, in addition to long-term memory deficit, the short-term memory deficit resultant from maternal deprivation in object recognition and aversive memory tasks is also prevented by physical exercise. Additionally, one of the mechanisms by which the physical exercise influences the memory processes involves its effects attenuating the oxidative damage in the maternal deprived rats' hippocampus and prefrontal cortex.

Memory for emotional material in temporal lobe epilepsy.

Several studies suggest that highly emotional information could facilitate long-term memory encoding and consolidation processes via an amygdala-hippocampal network. Our aim was to assess emotional perception and episodic memory for emotionally arousing material in patients with temporal lobe epilepsy (TLE) who are candidates for surgical treatment. We did this by using an audiovisual paradigm. Forty-six patients with medically resistant TLE (26 with left TLE and 20 with right TLE) and 19 healthy controls were assessed with a standard narrative test of emotional memory. The experimental task consisted of sequential picture slides with an accompanying narrative depicting a story that has an emotional central section. Subjects were asked to rate their emotional arousal reaction to each stimulus after the story was shown, while emotional memory (EM) was assessed a week later with a multiple choice questionnaire and a visual recognition task. Our results showed that ratings for emotional stimuli for the patients with TLE were significantly higher than for neutral stimuli (p=0.000). It was also observed that patients with TLE recalled significantly less information from each slide compared with controls, with a trend to lower scores on the questionnaire task for the group with LTLE, as well as poorer performance on the visual recognition task for the group with RLTE. Emotional memory was preserved in patients with RTLE despite having generally poorer memory performance compared with controls, while it was found to be impaired in patients with LTLE.

Autobiographical memory and hyperassociativity in the dreaming brain: implications for memory consolidation in sleep.

In this paper we argue that autobiographical memory (AM) activity across sleep and wake can provide insight into the nature of dreaming, and vice versa. Activated memories within the sleeping brain reflect one’s personal life history (autobiography). They can appear in largely fragmentary forms and differ from conventional manifestations of episodic memory. Autobiographical memories in dreams can be sampled from non-REM as well as REM periods, which contain fewer episodic references and become more bizarre across the night. Salient fragmented memory features are activated in sleep and re-bound with fragments not necessarily emerging from the same memory, thus de-contextualizing those memories and manifesting as experiences that differ from waking conceptions. The constructive nature of autobiographical recall further encourages synthesis of these hyper-associated images into an episode via recalling and reporting dreams. We use a model of AM to account for the activation of memories in dreams as a reflection of sleep-dependent memory consolidation processes. We focus in particular on the hyperassociative nature of AM during sleep.

Sleep and Alzheimer’s Disease

In the normal aging process, sleep changes accompany with increasing sleep fragmentation, nighttime awakenings and greater tendency for daytime sleep. Dementia provokes further deterioration of sleep patterns.1 The prevalence of Alzheimer’s disease (AD), most common form, is rapidly increasing and will probably accelerate dramatically within the next decades as a numbers of people are getting older. Although AD is usually recognized as progressive debilitation of memory, language, and intellect, sleep disturbance is a prevailing and often highly disruptive behavioral symptom associated with AD.2,3 At an early phase of the AD, these neuro behavioral symptoms may appear but seem to be usually associated with a more severe cognitive decline.3,4 The origin of sleep disturbances in AD is considered to be multifactorial. Sleep alterations occur with degeneration of neural pathways that modulate sleep-wake patterns and sleep architecture as well as other environmental factors.3,5 In return, cognitive symptoms may deteriorate through impairment of amyloid-β (Aβ) diurnal pattern and sleep-dependent memory consolidation processes by sleep disorders.6,7 Additionally, a correlation between sleep characteristics and cognitive decline in the elderly has been shown, focusing the fact that sleep and cognition are closely related.8-10 This article will review sleep changes with normal aging and AD, bidirectional relationship between sleep and AD pathology, and underlying mechanism. The result of sleep disturbances in AD will be discussed thereafter. Finally, recommendations as to areas in which future research is needed will be proposed. Received: October 23, 2014 Revised: April 3, 2015 Accepted: April 22, 2015

The Synergistic Relationship between Alzheimer's Disease and Sleep Disorders: An Update.

Sleep disorders are frequently reported in Alzheimer's disease (AD), with a significant impact on patients and caregivers and a major risk factor for early institutionalization. Although changes in sleep organization are a hallmark of the normal aging processes, sleep macro- and micro-architectural alterations are more evident in patients affected by AD. Degeneration of neural pathways regulating sleep-wake patterns and sleep architecture may contribute to sleep alterations. In return, several recent studies suggested that common sleep disorders may precede clinical symptoms of dementia and represent risk factors for cognitive decline, through impairment of sleep-dependent memory consolidation processes. Thus, a close relationship between sleep disorders and AD has been largely hypothesized. Here, sleep alterations in AD and its pre-dementia stage, mild cognitive impairment, and their complex interactions are reviewed.

Different temporal patterns of memory incorporations into dreams for laboratory and virtual reality experiences: relation to dreamed locus of control

Previous work demonstrates that memories about a target experience are incorporated into dream content according to a U-shaped temporal pattern with a peak of incorporations around 1-2 days following the experience (day-residue effect), a diminution on days 3-4, and a recurrence of incorporations on days 5-7 (dream-lag effect). This temporal pattern has been observed for many types of experiences, but no study has yet investigated either whether the pattern occurs differentially for qualitatively distinct, yet temporally proximal, experiences or whether the pattern also manifests by generic changes not specifically related to the target memory. The current study traced memory source incorporation patterns of two qualitatively distinct but temporally overlapping events: a laboratory overnight stay (LAB), considered to be an interpersonal and passive experience; and a virtual reality maze task (VR), considered to be a solitary and active experience. Hypotheses were that: 1) elements of LAB and VR experiences would be incorporated independently and exhibit different temporal patterns of incorporation into dream content; and 2) these incorporation patterns would be associated with different generic changes in dream content, i.e., a primarily external dreamed Locus of Control (Dream LoC) for dreams incorporating LAB experiences and a primarily internal Dream LoC for dreams incorporating VR experiences. Twenty-six participants each spent 1 night in the sleep laboratory, underwent a VR maze task in the morning, and then kept a home dream log for 10 days. Judges rated dreams for evidence of incorporation of LAB and VR experiences. Results were consistent with expectations: 1) LAB and VR experiences showed independent and opposite temporal incorporation patterns; LAB incorporations showed both day-residue and dream-lag effects whereas VR incorporations revealed a peak only on day 4; 2) Dream LoC scores were more external for Day 1 (peak of LAB incorporations), and more internal for Day 4 (peak of VR incorporations). Different incorporation patterns for these two experiences may reflect separate underlying processes of memory consolidation responding to different types of stimulus events. Further, temporal patterning of both specific dream incorporations and general dream content changes (LoC) may reflect qualitatively different aspects of episodic memory consolidation.

H2A.Z helps genes remember their history so we can remember ours.

Histone variant exchange is a novel epigenetic regulator of cognition. We speculate that H2A.Z, a variant of canonical histone H2A, exerts unique effects on transcription during distinct stages of memory formation, ultimately acting to maintain memory of previous transcriptional states and poise genes for re-activation. Hippocampus-dependent memory formation is initiated by transient expression of memory-related genes, which support the storage of recently acquired memories. Soon after, memories undergo systems consolidation, which transfers memories from the hippocampus to the cortex for long-term storage, and requires ongoing re-activation of memory-related genes. We speculate that learning-induced H2A.Z eviction from nucleosomes initially contributes to stimulus-induced transcriptional induction needed for the initial process of memory consolidation. During systems consolidation, we speculate that delayed incorporation of H2A.Z into nucleosomes of memory-related genes in the cortex is needed to poise genes for rapid re-activation, thus supporting the long-term process of memory stabilization.

Post-training, intrahippocampal HDAC inhibition differentially impacts neural circuits underlying spatial memory in adult and aged mice.

Converging evidence indicates that pharmacologically elevating histone acetylation using post-training, systemic or intrahippocampal, administration of histone deacetylase inhibitor (HDACi) can enhance memory consolidation processes in young rodents but it is not yet clear, whether such treatment is sufficient to prevent memory impairments associated with aging. To address this question, we used a 1-day massed spatial learning task in the water maze to investigate the effects of immediate post-training injection of the HDACi trichostatin A (TSA) into the dorsal hippocampus on long-term memory consolidation in 3-4 and 18-20 month-old mice. We show that TSA improved the 24 h-memory retention for the hidden platform location in young-adults, but failed to rescue memory impairments in older mice. The results further indicate that Young-TSA mice sacrificed 1 h after training had a robust increase in histone H4 acetylation in the dorsal hippocampal CA1 region (dCA1) and the dorsomedial part of the striatum (DMS), a structure important for spatial information processing. Importantly, TSA infusion in aged mice completely rescued altered H4 acetylation in the dCA1 but failed to alleviate age-associated decreased H4 acetylation in the DMS. Moreover, intrahippocampal TSA infusion produced concomitant decreases (in adults) or increases (in older mice) of acetylated histone levels in the ventral hippocampus (vCA1 and vCA3) and the lateral amygdala, two structures critically involved in stress and emotional responses. These data suggest that the failure of post-training, intrahippocampal TSA injection to reverse age-associated memory impairments may be related to an inability to recruit appropriate circuit-specific epigenetic patterns during early consolidation processes.

The hippocampus: A central node in a large-scale brain network for memory

The medial temporal lobe is a key region in the formation and consolidation of conscious or declarative memories. In this review, we will first consider the role of the hippocampus and its surrounding medial temporal lobe structures in recognition memory from a historical perspective. According to the dual process model of recognition memory, recognition judgments can be based on the recollection of details about previous presented stimuli or on the feeling of familiarity. Studies in humans, primates and rodents suggest that the hippocampus, the parahippocampal cortex and the perirhinal cortex play different roles in recollection and familiarity. Then, we will describe the role of the hippocampus and neocortex in memory consolidation: a process in which novel memories become integrated into long-term memory. After presenting possible mechanisms underlying sleep-dependent declarative memory consolidation, we will discuss the phenomenon of accelerated long-term forgetting. This type of memory deficit is often observed in epileptic patients with a hippocampal lesion, and provides a novel opportunity to investigate post-encoding and memory consolidation processes.