From creation to consolidation: a novel framework for memory processing

Long after playing squash, your brain continues to process the events that occurred during the game, thereby improving your game, and more generally, enhancing adaptive behavior. Understanding these mysterious processes may require novel theories

The functional role of dreaming in emotional processes

Dream experience (DE) represents a fascinating condition linked to emotional processes and the human inner world. Although the overlap between REM sleep and dreaming has been overcome, several studies point out that emotional and perceptually vivid contents are more frequent when reported upon awakenings from this sleep stage. Actually, it is well-known that REM sleep plays a pivotal role in the processing of salient and emotional waking-life experiences, strongly contributing to the emotional memory consolidation. In this vein, we highlighted that, to some extent, neuroimaging studies showed that the processes that regulate dreaming and emotional salience in sleep mentation share similar neural substrates of those controlling emotions during wakefulness. Furthermore, the research on EEG correlates of the presence/absence of DE and the results on EEG pattern related to the incorporated memories converged to assign a crucial role of REM theta oscillations in emotional re-processing. In particular, the theta activity is involved in memory processes during REM sleep as well as during the waking state, in line with the continuity hypothesis. Also, the gamma activity seems to be related to emotional processes and dream recall as well as to lucid dreams. Interestingly, similar EEG correlates of DE have been found in clinical samples when nightmares or dreams occur. Research on clinical samples revealed that promoting the rehearsal of frightening contents aimed to change them is a promising method to treat nightmares, and that lucid dreams are associated with an attenuation of nightmares. In this view, DE can defuse emotional traumatic memories when the emotional regulation and the fear extinction mechanisms are compromised by traumatic and frightening events. Finally, dreams could represent a sort of simulation of reality, providing the possibility to create a new scenario with emotional mastery elements to cope with dysphoric items included in nightmares. In addition, it could be hypothesized that the insertion of bizarre items besides traumatic memories might be functional to “impoverish” the negative charge of the experiences

Neuropsychological Generation of Source Amnesia: An Episodic Memory Disorder of the Frontal Brain

Source amnesia is an explicit memory (declarative) disorder, particularly episodic, where source or contextual information concerning facts is severely distorted and/or unable to be recalled. This paper reviews the literature on source amnesia, including memory distrust syndrome, and its accepted correlation with the medial diencephalic system and the temporal lobes, and the suggested linkage between the frontal lobes, including special interest with the prefrontal cortex. Posthypnotic induction was the first presentation of source amnesia identified in the literature. The Wisconsin Cart Sorting Test (WCST), Positron Emission Topography (PET), Phonemic Verbal Fluency Test, Stroop Color Word Interference Test, and explicit and implicit memory tests are defined and linked to empirical research on amnesiacs

Low-frequency oscillatory correlates of auditory predictive processing in cortical-subcortical networks: a MEG-study

Emerging evidence supports the role of neural oscillations as a mechanism for predictive information processing across large-scale networks. However, the oscillatory signatures underlying auditory mismatch detection and information flow between brain regions remain unclear. To address this issue, we examined the contribution of oscillatory activity at theta/alpha-bands (4–8/8–13 Hz) and assessed directed connectivity in magnetoencephalographic data while 17 human participants were presented with sound sequences containing predictable repetitions and order manipulations that elicited prediction-error responses. We characterized the spectro-temporal properties of neural generators using a minimum-norm approach and assessed directed connectivity using Granger Causality analysis. Mismatching sequences elicited increased theta power and phase-locking in auditory, hippocampal and prefrontal cortices, suggesting that theta-band oscillations underlie prediction-error generation in cortical-subcortical networks. Furthermore, enhanced feedforward theta/alpha-band connectivity was observed in auditory-prefrontal networks during mismatching sequences, while increased feedback connectivity in the alpha-band was observed between hippocampus and auditory regions during predictable sounds. Our findings highlight the involvement of hippocampal theta/alpha-band oscillations towards auditory prediction-error generation and suggest a spectral dissociation between inter-areal feedforward vs. feedback signalling, thus providing novel insights into the oscillatory mechanisms underlying auditory predictive processing

Acute Alcohol and Cognition: Remembering What It Causes Us to Forget

Addiction has been conceptualized as a specific form of memory that appropriates typically adaptive neural mechanisms of learning to produce the progressive spiral of drug-seeking and drug-taking behavior, perpetuating the path to addiction through aberrant processes of drug-related learning and memory. From that perspective, to understand the development of alcohol use disorders it is critical to identify how a single exposure to alcohol enters into or alters the processes of learning and memory, so that involvement of and changes in neuroplasticity processes responsible for learning and memory can be identified early on. This review characterizes the effects produced by acute alcohol intoxication as a function of brain region and memory neurocircuitry. In general, exposure to ethanol doses that produce intoxicating effects causes consistent impairments in learning and memory processes mediated by specific brain circuitry, whereas lower doses either have no effect or produce a facilitation of memory under certain task conditions. Therefore, acute ethanol does not produce a global impairment of learning and memory, and can actually facilitate particular types of memory, perhaps particular types of memory that facilitate the development of excessive alcohol use. In addition, the effects on cognition are dependent on brain region, task demands, dose received, pharmacokinetics, and tolerance. Additionally, we explore the underlying alterations in neurophysiology produced by acute alcohol exposure that help to explain these changes in cognition and highlight future directions for research. Through understanding the impact acute alcohol intoxication has on cognition, the preliminary changes potentially causing a problematic addiction memory can better be identified

Midazolam, hippocampal function, and transitive inference: Reply to Greene

The transitive inference (TI) task assesses the ability to generalize learned knowledge to new contexts, and is thought to depend on the hippocampus (Dusek & Eichenbaum, 1997). Animals or humans learn in separate trials to choose stimulus A over B, B over C, C over D and D over E, via reinforcement feedback. Transitive responding based on the hierarchical structure A > B > C > D > E is then tested with the novel BD pair. We and others have argued that successful BD performance by animals – and even humans in some implicit studies – can be explained by simple reinforcement learning processes which do not depend critically on the hippocampus, but rather on the striatal dopamine system. We recently showed that the benzodiazepene midazolam, which is thought to disrupt hippocampal function, profoundly impaired human memory recall performance but actually enhanced implicit TI performance (Frank, O'Reilly & Curran, 2006). We posited that midazolam biased participants to recruit striatum during learning due to dysfunctional hippocampal processing, and that this change actually supported generalization of reinforcement values. Greene (2007) questions the validity of our pharmacological assumptions and argues that our conclusions are unfounded. Here we stand by our original hypothesis, which remains the most parsimonious account of the data, and is grounded by multiple lines of evidence

Behavioral and Neural Correlates of Misses During Cued Recall

Recognition memory is thought to rely upon both recollection and familiarity. When people recall an episode from the past it is generally considered to reflect the memory process of recollection. Therefore, if people can successfully recall an item, they should be able to recognize it. However, in cued recall paradigms of memory research, participants sometimes correctly recall a studied target word in the presence of a strong semantic cue but then fail to recognize that word as actually having been studied. This paradox and underlying cognitive processes have been minimally studied by scientists, leaving this phenomenon poorly understood. Extant research has investigated some of the conditions necessary to produce these conditions but not the underlying neural correlates that drive them. The present study builds upon earlier studies using Electroencephalogram (EEG) to investigate the neural processes that underlie recognition failures of successfully recalled words. In the present experiment, participants studied words one at a time, and then later were asked to verbally recall these previously studied words as cued by their semantic associates. Following the participant’s verbal response, their recognition memory was tested for the recalled word. The current study aimed to use physiological measures (EEG) to investigate the explicit and implicit cognitive processes that may be involved in the recognition failure of recalled words. The data indicate that successfully recalled words that are recognized are driven by recollection at recall and a combination of recollection and familiarity at recognition, whereas successfully recalled words that are not recognized are instead driven by semantic priming at recall and at recognition, are driven by negative-going ERP effects reflecting implicit processes such as repetition fluency