Abstract Understanding the organizing principles of brain activity can advance neurotechnology and medical diagnosis. Traditionally, neural activity is viewed as consisting oscillations in distinct frequency bands. However, emerging evidence suggests these oscillations often manifest as transient bursts rather than sustained rhythms. We examine the hypothesis that rhythmicity (sustained vs bursty) adds a further dimension to brain organization. Using a rhythmicity measure, we segment neurophysiological spectra from 859 participants across datasets, species, recording techniques, ages 18–88, sexes, brain regions, and cognitive states in health and disease. Our results reveal a universal rhythmicity-resolved spectral architecture with two categories: high-rhythmicity bands exhibiting sustained oscillations and new low-rhythmicity bands dominated by brief bursts. This architecture reflects two modes of operation: sustained bands suitable for maintaining ongoing activity, and transient bands which can signal responses to change. The rhythmicity-resolved architecture provides a unifying framework that bridges human and non-human findings, enables individualized spectral definitions, and offers a principled basis for understanding brain activity.

Traditional approaches probe cognition by aligning brain activity to external stimuli. Building on evidence that transient oscillatory activity marks neural responses, we articulate burst-related potentials (BRPs) as temporal anchors for studying cognitive processes poorly captured by stimulus-locked analyses.

Suppressing retrieval of a memory when faced with a reminder has been shown to reduce the probability of that memory coming to mind in the future, a phenomenon known as Suppression-Induced Forgetting (SIF). However, efforts to observe SIF have sometimes failed, leading some to question the robustness of the effect. To address this issue, we conducted a comprehensive meta-analysis of SIF within the Think/No-Think paradigm including several key methodological variants to the original design. Across 500 effects from 120 studies, we observed a consistent aggregate SIF effect (d ≈ 0.20 – 0.40) measured using either same probe (SIF ≈ 6%), independent probe (SIF ≈ 5-6%) or recognition (SIF ≈ 2-4%) tests. Notably, there was considerable methodological variability, and prediction intervals revealed substantial heterogeneity. Moderator analyses undertaken to explain this variability found SIF to be credibly larger when using (a) relatively more repetitions during the Think/No-Think phase within same probe data; (b) thought substitution instructions within same probe data (with the opposite observed for independent probe data); and, (c) autobiographical memories (or future worries) as opposed to words or images. Results provide compelling evidence of the SIF effect but also suggest areas for future expansion.

This chapter discusses what is known about successful storage of information in episodic memory. It focuses on basic cognitive and neuroscience research on the factors and mechanisms that contribute to good episodic memory in healthy participants. A key element of Bartlett's approach to memory was his emphasis on how people actively and inevitably seek meaning in new experiences, and, in doing so, impose their own organization on the events they perceive in the world, often through schemas. Participants' goal was to learn to recall as many words as they could, and to increase this amount over repetitions. Systems consolidation is thought to reflect the gradual elimination of the role of the hippocampus, and the progressive increase in importance of cortical representations in storing and retrieving an event, sometimes characterized as the transfer of memories to neocortex.

This chapter considers what is known about how people forget things that they would prefer not to remember. Motivated forgetting encompasses the term psychogenic amnesia, which means any forgetting that is psychological in origin, and not attributed to neurological damage or dysfunction—forgetting that is psychological in genesis. Theoretically, controlling unwanted memories may be accomplished by intervening at any stage of memory. The simplest way to avoid remembering unpleasant events is to limit their encoding. People seem to regulate their memory to protect their self-image, especially when feedback poses high levels of threat to that image. List-method directed forgetting illustrates how when people no longer wish to remember events, they can intentionally reduce their accessibility. Hypermnesia is largest on free recall tests but has been found on cued recall and recognition tests.

Controlling action and thought requires the capacity to stop mental processes. Over the past two decades, evidence has grown that a domain-general inhibitory control mechanism supported by the right lateral prefrontal cortex achieves these functions. However, current views of the neural mechanisms of inhibitory control derive largely from research into the stopping of action. Whereas action stopping is a convenient empirical model, it does not invoke thought inhibition and cannot be used to identify the unique features of this process. Here, we review research that addresses how organisms stop a key process that drives thoughts: memory retrieval. This work has shown that retrieval stopping shares right dorsolateral and ventrolateral prefrontal mechanisms with action stopping, consistent with a domain-general inhibitory control mechanism, but also recruits a distinct fronto-temporal pathway that determines the success of mental control. As part of this pathway, GABAergic inhibition within the hippocampus influences the efficacy of prefrontal control over thought. These unique elements of mental control suggest that hippocampal disinhibition is a transdiagnostic factor underlying intrusive thinking, linking the fronto-temporal control pathway to preclinical models of psychiatric disorders and fear extinction. We suggest that retrieval-stopping deficits may underlie the intrusive thinking that is common across many psychiatric disorders. The capacity to prevent unwanted thoughts is important for cognitive function and mental health. Anderson et al. describe insights into the neural mechanisms of the inhibitory control of thought that have been gained from studies of retrieval stopping and discuss how this knowledge informs our understanding of psychiatric disorders associated with intrusive thinking.

Novel experiences appear to benefit memory for unrelated information encoded shortly before or after. Other research suggests that memory is impaired by effortful tasks following encoding, compared to simply resting. This registered report explicitly tested the proactive and retroactive effects of novel exploration and wakeful rest. Four groups of participants explored a novel or familiarised virtual environment, either shortly before or shortly after encoding a list of unrelated words. A fifth 'wakeful rest' group performed a low-effort attention task before and after encoding. Memory was tested with immediate free recall, delayed (next day) free recall and delayed recognition with confidence judgements (from which recollection and familiarity were estimated). Bayes factors provided evidence against both proactive and retroactive benefits of novelty across all measures of memory, but provided evidence for a retroactive benefit of rest for immediate recall. In exploratory analysis, we also found evidence for a proactive benefit of rest on immediate recall. We argue that the bidirectional benefits of wakeful rest are more easily explained by Temporal Distinctiveness theory than Consolidation theory. Overall, wakeful rest surrounding learning may represent a useful intervention for improving memory, while novel exploration may not.

Background. The mechanisms underlying generalized forms of dissociative ('psychogenic') amnesia are poorly understood. One theory suggests that memory retrieval is inhibited via prefrontal control. Findings from cognitive neuroscience offer a candidate mechanism for this proposed retrieval inhibition. By applying predictions based on these experimental findings, we examined the putative role of retrieval suppression in dissociative amnesia. Methods. We analyzed fMRI data from two previously reported cases of dissociative amnesia. Patients had been shown reminders from forgotten and remembered time periods (colleagues and school friends). We examined the neuroanatomical overlap between regions engaged in the unrecognized compared to the recognized condition, and the regions engaged during retrieval suppression in laboratory-based tasks. Effective connectivity analyses were performed to test the hypothesized modulatory relationship between the right anterior dorsolateral prefrontal cortex (raDLPFC) and the hippocampus. Both patients were scanned again following treatment, and analyses were repeated. Results. We observed substantial functional alignment between the inhibitory regions engaged during laboratory-based retrieval suppression tasks, and those engaged when patients failed to recognize their current colleagues. This included significant activation in the raDLPFC and right ventrolateral prefrontal cortex, and a corresponding deactivation across autobiographical memory regions (hippocampus, medial PFC). Dynamic causal modeling confirmed the hypothesized modulatory relationship between the raDLPFC and the hippocampus. This pattern was no longer evident following memory recovery in the first patient, but persisted in the second patient who remained amnesic. Conclusions. Findings are consistent with an inhibitory mechanism driving down activity across core memory regions to prevent the recognition of personally relevant stimuli.

Sleep disturbances are associated with intrusive memories, but the neurocognitive mechanisms underpinning this relationship are poorly understood. Here, we show that sleep deprivation disrupts prefrontal inhibition of memory retrieval, and that the overnight restoration of this inhibitory mechanism is associated with time spent in rapid eye movement (REM) sleep. The functional impairments arising from sleep deprivation are linked to a behavioral deficit in the ability to downregulate unwanted memories, and coincide with a deterioration of deliberate patterns of self-generated thought. We conclude that sleep deprivation gives rise to intrusive memories via the disruption of neural circuits governing mnemonic inhibitory control, which may rely on REM sleep.

Forgetting is a ubiquitous phenomenon that is actively promoted in many species. The act of remembering some experiences can cause the forgetting of others in both humans and rats. We previously found that when rats need to retrieve a memory to guide exploration, it reduces later retention of other competing memories encoded in that environment. As with humans, retrieval-induced forgetting (RIF) relies on prefrontal control processes, is competition-dependent, and is cue-independent. RIF is thought to be driven by inhibitory control signals from the prefrontal cortex that target areas where memories are stored. Serotonin plays a crucial role in behaviors requiring high cognitive demand, including memory processes, partly through its modulation of Prefrontal Cortex activity. However, its potential involvement in regulating forgetting remains unexplored. Here, we exposed rats to the RIF tssk and employed a pharmacological approach to manipulate the activity and signaling of serotonin receptors 5-HT1A, 5-HT2A, and 5-HT2C in the medial prefrontal cortex (mPFC) of rats, as well as to inhibit downstream effectors. Our findings reveal a distinct role for prefrontal serotonin signaling in RIF. While 5-HT2C receptor manipulation had no effect, blocking 5-H21A or 5-HT2A receptors in the mPFC abolished RIF, demonstrating their necessity in this process. Strikingly, further analysis identified the PI3K/AKT pathway as a key downstream effector of 5-HT2A receptor activation, suggesting a specific molecular mechanism through which serotonin modulates inhibitory control over memory. These results uncover a previously unrecognized serotonergic modulation of adaptive forgetting, linking prefrontal serotonin signaling to the regulation of memory competition. ### Competing Interest Statement The authors have declared no competing interest.

This chapter considers the mechanisms that underlie forgetting. The apparent flattening out of the forgetting curve over time demonstrates that memories are not equally vulnerable to forgetting at all points in their history. Experimental psychologists have traditionally emphasized incidental forgetting, stressing the involvement of passive processes that occur as a bi-product of changes in the world or the person. Retrieval-induced forgetting is usually studied with the retrieval practice paradigm. Associative unlearning is theoretical account of interference effects, which can be illustrated intuitively with a real-life example. Research on retrieval-induced forgetting suggests that selectively retrieving facts or events places demands on attentional control processes like inhibition, to overcome interference from distracting memories.

Selective retrieval of a target memory often triggers inhibitory control to reduce competition from related traces, a process that induces forgetting of the competing content. It is unknown, however, whether inhibition during selective retrieval specifically targets a competitor's episodic representation or instead extends to its affective components. Here we report evidence in humans that selective retrieval of a neutral memory not only diminishes access to the mnemonic content of unpleasant competing memories, but also alters their emotional character. Memory and emotion suppression effects were accompanied by reduced neural activation and weakened representational patterns unique to competing memories in the VTC and amygdala respectively, in an independent fashion. Selective retrieval engaged the left VLPFC, which decreased in activity over repeated retrievals of the same memory, as competition from the unpleasant scene was resolved. This left VLPFC region colocalizes with key prefrontal regions engaged during cognitive reappraisal, suggesting that selective retrieval's impact on affective responses may contribute to reappraisal's benefits. These findings indicate that inhibitory control during selective retrieval affects both mnemonic and affective representations, providing a novel mechanistic basis for a well-known emotion regulation practice. ### Competing Interest Statement The authors have declared no competing interest.

Retrieval stopping, the intentional suppression of unwanted memories, plays a critical role in emotion regulation and cognitive control, yet little is known about its function in adolescence. Using an autobiographical Think/No-Think paradigm, we investigated whether adolescents can control the retrieval of personal emotional events. Forty-nine adolescent participants (13-17) generated positive and negative autobiographical memories for retrieval or suppression in the Think/No-Think task. Memory accuracy and vividness were assessed before and after. Adolescents showed suppression-induced forgetting: negative memories were recalled less accurately and more slowly. Vividness ratings declined for suppressed memories, but not significantly more than negative baseline memories, suggesting a spill-over effect of retrieval stopping to all negative memories, rather than an effect confined to the suppressed negative memories. Overall, the results provide evidence that adolescents can intentionally suppress autobiographical emotional memories. These findings extend investigations in adults by showing inhibitory control over memory retrieval is functional during adolescence, a critical period for emotion regulation. The flexibility that the autobiographical TNT task offers allows it to be extended to fears or worries, offering a promising avenue for applied research. Future research should examine its potential as a scalable, low-cost supplement to therapy, supporting emotion regulation and mental health in youth.

The act of recalling memories can paradoxically lead to the forgetting of other associated memories, a phenomenon known as retrieval-induced forgetting (RIF). Inhibitory control mechanisms, primarily mediated by the prefrontal cortex, are thought to contribute to RIF. In this study, we examined whether stimulating the medial prefrontal cortex (mPFC) with transcranial direct current stimulation modulates RIF and investigated the associated electrophysiological correlates. In a randomized study, 50 participants (27 males and 23 females) received either real or sham stimulation before performing retrieval practice on target memories. After retrieval practice, a final memory test to assess RIF was administered. We found that stimulation selectively increased the retrieval accuracy of competing memories, thereby decreasing RIF, while the retrieval accuracy of target memories remained unchanged. The reduction in RIF was associated with a more pronounced beta desynchronization within the left dorsolateral prefrontal cortex (left-DLPFC), in an early time window (<500 ms) after cue onset during retrieval practice. This led to a stronger beta desynchronization within the parietal cortex in a later time window, an established marker for successful memory retrieval. Together, our results establish the causal involvement of the mPFC in actively suppressing competing memories and demonstrate that while forgetting arises as a consequence of retrieving specific memories, these two processes are functionally independent. Our findings suggest that stimulation potentially disrupted inhibitory control processes, as evidenced by reduced RIF and stronger beta desynchronization in fronto-parietal brain regions during memory retrieval, although further research is needed to elucidate the specific mechanisms underlying this effect.

The ability to stop unwanted memories from coming to mind is theorised to be essential for maintaining good mental health. People can employ intentional strategies to prevent conscious intrusions of negative memories, and repeated attempts to stop retrieval both reduces the frequency of intrusions and improves subsequent emotions elicited by those memories. However, it is still unknown whether memory control can improve negative emotions immediately, at the time control is attempted. It is also not clear which strategy is most beneficial for emotion regulation; clearing the mind of any thoughts of negative memories via direct suppression, or substituting memory recall with alternative thoughts. Here, we provide novel evidence that memory control immediately regulates negative emotions associated with autobiographical memories of morally wrong actions. Repeated control significantly improved negative emotions over time, regardless of the strategy used to implement control. Thought substitution involving either positive diversionary thinking or counterfactual thinking both induced positive feelings, whereas direct suppression neutralised emotions, regardless of whether memories were positive or negative. These empirical findings have implications for clinical practice as they indicate that memory control strategies could be effective emotion regulation methods for real-world intrusive memories.

Structural damage to the hippocampus gives rise to a severe memory deficit for personal experiences known as organic amnesia. Remarkably, such structural damage may not be the only way of creating amnesia; windows of amnesia can also arise when people deliberately disengage from memory via a process known as retrieval suppression. In this review, we discuss how retrieval suppression induces systemic inhibition of the hippocampus, creating "amnesic shadow" intervals in people's memory for their personal experiences. When new memories are encoded or older memories are reactivated during this amnesic shadow, these memories are disrupted, and such disruption even arises when older memories are subliminally cued. Evidence suggests that the systemic inhibition of the hippocampus during retrieval suppression that gives rise to the amnesic shadow may be mediated by engagement of hippocampal GABAergic inhibitory interneurons. Similar amnesic shadow effects are observed during working memory tasks like the n-back, which also induce notable hippocampal downregulation. We discuss our recent proposal that cognitive operations that require the disengagement of memory retrieval, such as retrieval suppression, are capable of mnemonic process inhibition (the inhibition of mnemonic processes such as encoding, consolidation, and retrieval and not simply individual memories). We suggest that people engage mnemonic process inhibition whenever they shift attention from internal processes to demanding perceptual-motor tasks that may otherwise be disrupted by distraction from our inner world. This hitherto unstudied model of inhibition is a missing step in understanding what happens when attentional shifts occur between internally and externally oriented processes to facilitate goal-directed behaviour. This process constitutes an important novel mechanism underlying the forgetting of life events.

The act of recalling memories can paradoxically lead to the forgetting of other associated memories, a phenomenon known as retrieval-induced forgetting (RIF). This effect is thought to be mediated by inhibitory control mechanisms in the prefrontal cortex of the brain. Here we investigated whether stimulation of the medial prefrontal cortex (mPFC) with transcranial direct current stimulation modulates inhibitory control during memory retrieval in a RIF paradigm. In a randomized study, fifty participants received either real or sham stimulation, before performing retrieval practice on target memories. After retrieval practice, a final test was administered to measure the impact of stimulation on RIF. We found that stimulation selectively increased the retrieval accuracy of non-target memories and thus decreased RIF, suggesting a disruption of inhibitory control. Meanwhile, no change arose for the retrieval accuracy of target memories. The reduction in RIF was caused by a more pronounced beta desynchronization within the left dorsolateral prefrontal cortex (left-DLPFC), in an early time window (<500 msec) after the onset of the cue during retrieval practice. This, in turn, led to a stronger beta desynchronization within the parietal cortex in a later time window, an established marker for successful memory retrieval. Together, our results establish the causal involvement of the mPFC in actively suppressing competing memories and we demonstrate that while forgetting arises as a consequence of retrieving specific memories, these two processes are functionally independent. Finally, we demonstrate that beta desynchronization in the fronto-parietal brain regions indicates the disruption of inhibitory control.### Competing Interest StatementThe authors have declared no competing interest.

When reminded of an unpleasant experience, people often try to exclude the unwanted memory from awareness, a process known as retrieval suppression. Here we used multivariate decoding (MVPA) and representational similarity analyses on EEG data to track how suppression unfolds in time and to reveal its impact on item-specific cortical patterns. We presented reminders to aversive scenes and asked people to either suppress or to retrieve the scene. During suppression, mid-frontal theta power within the first 500 ms distinguished suppression from passive viewing of the reminder, indicating that suppression rapidly recruited control. During retrieval, we could discern EEG cortical patterns relating to individual memories-initially, based on theta-driven visual perception of the reminders (0 to 500 ms) and later, based on alpha-driven reinstatement of the aversive scene (500 to 3000 ms). Critically, suppressing retrieval weakened (during 360 to 600 ms) and eventually abolished item-specific cortical patterns, a robust effect that persisted until the reminder disappeared (780 to 3000 ms). Representational similarity analyses provided converging evidence that retrieval suppression weakened the representation of target scenes during the 500 to 3000 ms reinstatement window. Together, rapid top-down control during retrieval suppression abolished cortical patterns of individual memories, and precipitated later forgetting. These findings reveal a precise chronometry on the voluntary suppression of individual memories.