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High-frequency oscillatory events, termed ripples, represent synchrony of neural activity in the brain. Recent evidence suggests that medial temporal lobe (MTL) ripples support memory retrieval. However, it is unclear if ripples signal the reinstatement of episodic memories. Analyzing electrophysiological MTL recordings from 245 neurosurgical participants performing episodic recall tasks, we find that the rate of hippocampal ripples rises just prior to the free recall of recently formed memories. This prerecall ripple effect (PRE) is stronger in the CA1 and CA3/dentate gyrus (CA3/DG) subfields of the hippocampus than the neighboring MTL regions entorhinal and parahippocampal cortex. PRE is also stronger prior to the retrieval of temporally and semantically clustered, as compared with unclustered, recalls, indicating the involvement of ripples in contextual reinstatement, which is a hallmark of episodic memory.

We present a framework for understanding the effects of automation and other types of technological changes on labor demand, and use it to interpret changes in US employment over the recent past. At the center of our framework is the allocation of tasks to capital and labor—the task content of production. Automation, which enables capital to replace labor in tasks it was previously engaged in, shifts the task content of production against labor because of a displacement effect. As a result, automation always reduces the labor share in value added and may reduce labor demand even as it raises productivity. The effects of automation are counterbalanced by the creation of new tasks in which labor has a comparative advantage. The introduction of new tasks changes the task content of production in favor of labor because of a reinstatement effect, and always raises the labor share and labor demand. We show how the role of changes in the task content of production—due to automation and new tasks—can be inferred from industry-level data. Our empirical decomposition suggests that the slower growth of employment over the last three decades is accounted for by an acceleration in the displacement effect, especially in manufacturing, a weaker reinstatement effect, and slower growth of productivity than in previous decades.

Memory retrieval allows us to reinstate previously encoded information but is also considered to contribute to memory enhancement. Retrieval-induced enhancement may involve processing to strengthen memory traces, but neural processing beyond reinstatement during retrieval remains elusive. Here, we show that hippocampal processing, different from memory reinstatement, exists during retrieval in the human brain. By tracking changes in the response patterns in the selected hippocampal and cortical regions over time during retrieval based on functional MRI, we found that the representation of associative memory in CA3/DG became stronger even after cortical memory reinstatement, while CA1 showed significant memory representation at retrieval onset with the cortical reinstatement, but not afterwards. This tendency was not observed in the condition without active retrieval. Moreover, subsequent long-term memory performance depended on the delayed CA3/DG representation during retrieval. These findings suggest that CA3/DG contributes to neural processing beyond memory reinstatement during retrieval, which may lead to memory enhancement.

Alcohol use disorder (AUD) remains a significant problem in the United States, resulting in over 178,000 alcohol-related deaths annually. A central problem in treating AUD is the high rate of relapse to alcohol use even after protracted periods of abstinence. Stress is a major contributor to the chronic relapsing and compulsive nature of AUD, and it alters neurocircuitry mediating craving and drug seeking. Chronic alcohol use dysregulates the neuropeptides orexin (OX)/hypocretin and dynorphin (DYN), which contribute to alcohol seeking and relapse. OX neurons originate exclusively in the hypothalamus and co-express DYN. Although OX and DYN are localized in the same synaptic vesicles and co-released when the hypothalamus is stimulated, they play opposing roles in reward, motivation, and substance use. OX, via OX receptor (OXR) signaling, promotes reward-seeking behavior, whereas DYN, acting through κ-opioid receptors (KOPs), increases depressive-like states and plays a key role in mediating aversive effects of stress. OX neurons densely innervate the paraventricular nucleus of the thalamus (PVT), a brain region that is involved in the regulation of reward function, stress, anxiety, and drug-directed behavior. In individuals with AUD, chronic alcohol use damages the thalamus, resulting in volume reductions and cognitive deficits. Therefore, lasting changes in PVT OX/DYN transmission and their interaction following chronic alcohol use may underlie stress-induced alcohol craving and relapse. Although their opposing roles in the PVT are established, implications of their interaction, particularly under conditions of stress, are limited in the context of alcohol use and reinstatement. This review synthesizes evidence from preclinical evidence and complementary clinical observations that implicate the co-transmission of OX and DYN in the PVT, with an emphasis on the posterior PVT (pPVT), which receives the most OX afferents, during the stress-induced reinstatement of alcohol seeking. We also discuss the potential of targeting OXRs and KOPs pharmacologically to reduce stress-induced alcohol craving and reinstatement. This review will help disentangle individual vs. interactive contributions of OX and DYN, and elucidate how their modulation within stress- and reward-related circuits may reveal novel insights for preventing relapse in individuals with AUD.

Mnemonic decision-making has long been hypothesized to rely on hippocampal dynamics that bias memory processing toward the formation of new memories or the retrieval of old ones. Successful memory encoding may be best optimized by pattern separation, whereby two highly similar experiences can be represented by underlying neural populations in an orthogonal manner. By contrast, successful memory retrieval is thought to be supported by a recovery of the same neural pattern laid down during encoding. Here we examined how hippocampal pattern completion and separation emerge over time during memory decisions. We measured electrocorticography activity in the human hippocampus and posterior occipitotemporal cortex (OTC) while participants performed continuous recognition of items that were new, repeated (old), or highly similar to a prior item (similar). During retrieval decisions of old items, both regions exhibited significant reinstatement of multivariate high-frequency activity (HFA) associated with encoding. Further, the extent of reinstatement of encoding patterns during retrieval was correlated with the strength (HFA power) of hippocampal encoding. Evidence for encoding pattern reinstatement was also seen in OTC on trials requiring fine-grained discrimination of similar items. By contrast, hippocampal activity showed evidence for pattern separation during these trials. Together, these results underscore the critical role of the hippocampus in supporting both reinstatement of overlapping information and separation of similar events.

What are the brain mechanisms responsible for episodic memory retrieval? Norman et al. investigated epilepsy patients who had electrodes implanted in the hippocampus and a variety of cortical areas. Using a visual learning paradigm, they examined the temporal relationship between the incidence of hippocampal sharp-wave ripples and recall. Effective encoding of visual information was associated with higher incidence of ripples. Successful recall was preceded by an increased probability of ripples, which were also associated with transient reemergence of activation patterns in higher visual cortical areas. Hippocampal ripples may thus boost recollections during episodic memory retrieval. Science , this issue p. eaax1030 Ripples reinstate human memory during free recall. Hippocampal sharp-wave ripples (SWRs) constitute one of the most synchronized activation events in the brain and play a critical role in offline memory consolidation. Yet their cognitive content and function during awake, conscious behavior remains unclear. We directly examined this question using intracranial recordings in human patients engaged in episodic free recall of previously viewed photographs. Our results reveal a content-selective increase in hippocampal ripple rate emerging 1 to 2 seconds prior to recall events. During recollection, high-order visual areas showed pronounced SWR-coupled reemergence of activation patterns associated with recalled content. Finally, the SWR rate during encoding predicted subsequent free-recall performance. These results point to a role for hippocampal SWRs in triggering spontaneous recollections and orchestrating the reinstatement of cortical representations during free episodic memory retrieval.

Age-related episodic memory decline is characterized by striking heterogeneity across individuals. Hippocampal pattern completion is a fundamental process supporting episodic memory. Yet, the degree to which this mechanism is impaired with age, and contributes to variability in episodic memory, remains unclear. We combine univariate and multivariate analyses of fMRI data from a large cohort of cognitively normal older adults (N=100) to measure hippocampal activity and cortical reinstatement during retrieval of trial-unique associations. Trial-wise analyses revealed that (a) hippocampal activity scaled with reinstatement strength, (b) cortical reinstatement partially mediated the relationship between hippocampal activity and associative retrieval, (c) older age weakened cortical reinstatement and its relationship to memory behaviour. Moreover, individual differences in the strength of hippocampal activity and cortical reinstatement explained unique variance in performance across multiple assays of episodic memory. These results indicate that fMRI indices of hippocampal pattern completion explain within- and across-individual memory variability in older adults.

For confidence of memory, a neural basis such as traces of stored memories should be required. However, because false memories have never been stored, the neural basis for false memory confidence remains unclear. Here we monitored the brain activity in participants while they viewed learned or novel objects, subsequently decided whether each presented object was learned and assessed their confidence levels. We found that when novel objects are presented, false memory confidence significantly depends on the shared representations with learned objects in the prefrontal cortex. However, such a tendency was not found in posterior regions including the visual cortex, which may be involved in the processing of perceptual gist. Furthermore, the confidence-dependent shared representations were not observed when participants correctly answered novel objects as non-learned objects. These results demonstrate that false memory confidence is critically based on the reinstatement of high-level semantic gist of stored memories in the prefrontal cortex.

It is widely assumed that context reinstatement benefits memory, but our experiments revealed that context reinstatement can systematically distort memory. Participants viewed pictures of objects superimposed over scenes, and we later tested their ability to differentiate these old objects from similar new objects. Context reinstatement was manipulated by presenting objects on the reinstated or switched scene at test. Not only did context reinstatement increase correct recognition of old objects, but it also consistently increased incorrect recognition of similar objects as old ones. This false recognition effect was robust, as it was found in several experiments, occurred after both immediate and delayed testing, and persisted with high confidence even after participants were warned to avoid the distorting effects of context. To explain this memory illusion, we propose that context reinstatement increases the likelihood of confusing conceptual and perceptual information, potentially in medial temporal brain regions that integrate this information.