Neurobiology of Learning and Memory最新文献

{"title":"Erratum to “C57BL/6 mouse substrain differences in the ontogeny of auditory fear” [Neurobiol. Learn. Memory 225 (2026) 108165]","authors":"Hanista Premachandran, Kanza Naveed, Maithe Arruda-Carvalho","doi":"10.1016/j.nlm.2026.108202","DOIUrl":"10.1016/j.nlm.2026.108202","url":null,"abstract":"","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"227 ","pages":"Article 108202"},"PeriodicalIF":2.1,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"No evidence for a protein-synthesis-dependent form of long-term fear memory: Translational inhibition and neural inactivation disrupt short- and long-term memory measures to the same degree","authors":"S. Al-Smadi, L.A. Rimstad, C.J. Scavuzzo, D. Treit, C.T. Dickson","doi":"10.1016/j.nlm.2026.108186","DOIUrl":"10.1016/j.nlm.2026.108186","url":null,"abstract":"<div><div>Translational inhibition has been suggested to impair long-term memory (LTM) while leaving short-term memory (STM) unaffected. However, intracranial infusions of protein synthesis inhibitors such as anisomycin (ANI), cycloheximide, and emetine have been shown to profoundly suppress both spontaneous and evoked neural activity, likely due to impairments of mitochondrial function and cellular metabolic loss. Given this neural suppressive effect, we wanted to re-examine the influence of translational inhibition on acquiring and retaining novel information with a direct comparison to agents that simply inactivate neural activity (without affecting protein synthesis). Our model was the widely-used cued-fear conditioning paradigm which is known to be dependent on the basolateral amygdala complex (BLA). Using male rats, we compared the behavioral deficits in cue fear conditioning induced by intra-BLA infusions of ANI to other commonly used neural inactivators, including the GABA<sub>A</sub> agonist muscimol (MUSC) and the sodium channel blocker tetrodotoxin (TTX). We confirmed that intra-BLA infusions of ANI and MUSC suppressed neural activity by examining effects on spiking activity in the BLA. In behavioral experiments, pre-training bilateral BLA infusions of ANI impaired both short-term (2 h) and long-term (24 h) cue fear memory similarly to the effects observed with both MUSC and TTX. Our results suggest that reductions in neural activity, whether via GABA<sub>A</sub> agonism, sodium channel blockade, or translational inhibition, are essential for both short- and long-term memory. Consequently, the influence of translational inhibitors may be better understood as being mediated via neural inactivation rather than solely the result of the absence of <em>de novo</em> synthesis of plasticity-related proteins. Previous work that interprets results using translational inhibitors as being <em>purely protein-synthesis-dependent</em> must to be reconsidered.</div></div><div><h3>Significance statement</h3><div>The axiomatic idea that protein synthesis can distinguish between phases of memory, namely short- versus long-term forms, is entirely based on work purporting to show differential disruptive effects of translational inhibitors on retrieval tested at long, but not short-term delays. However, protein synthesis inhibitors profoundly suppress neural activity as well, which should have an equivalent detrimental effect on both short- and long-term memory. In this study, we demonstrate that the translational inhibitor anisomycin suppresses neural activity in the basolateral amygdala which results in deficits in both short- and long-term memory for conditioned fear, similarly to agents that ONLY block neural activity. These findings are consistent with an important and under-appreciated role of neural activity in memory processes and argue for a critical re-evaluation of the strict <em>de novo</em> protein hypothesis of memory consolidation.</div></di","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"226 ","pages":"Article 108186"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148295772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Dynamic regulation of neuronal vault trafficking and RNA cargo by the noncoding RNA, Vaultrc5” [Neurobiol. Learn. Memory 225 (2026) 108161]","authors":"Mason R.B. Musgrove, Laura J. Leighton, Margaux Lebouc, Wei-Siang Liau, Alexander D. Walsh, Paul R. Marshall, Stephanie M. Heyworth, Adekunle T. Bademosi, Nathalie Hertrich, Qiongyi Zhao, Sachithrani U. Madugalle, Ambika Periyakaruppiah, Xiang Li, Joshua W.A. Davies, Haobin Ren, Hao Gong, Esmi L. Zajaczkowski, Nathalie Dehorter, Frederic A. Meunier, Marina Mikhaylova, Timothy W. Bredy","doi":"10.1016/j.nlm.2026.108182","DOIUrl":"10.1016/j.nlm.2026.108182","url":null,"abstract":"","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"226 ","pages":"Article 108182"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148302456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemogenetic disruption of the hippocampus impairs gustatory preconditioning in rats","authors":"Mélie M. Talaron,&nbsp;Nathan M. Holmes,&nbsp;Guillaume Ferreira,&nbsp;Etienne Coutureau","doi":"10.1016/j.nlm.2026.108187","DOIUrl":"10.1016/j.nlm.2026.108187","url":null,"abstract":"<div><div>Adaptive behavior often relies on learning associations between stimuli that were never directly paired with reinforcement. Sensory preconditioning provides a powerful paradigm to investigate such indirect learning: when neutral stimuli A and X are paired during preconditioning, and X is subsequently paired with an unconditioned stimulus (US) during conditioning, stimulus A elicits conditioned response at test despite never being directly paired with the US. While the hippocampus is known to be critical for this process, its involvement in unimodal sensory preconditioning remains unclear. Here, we investigated the role of the hippocampus (dorsal and ventral) during different phases of gustatory preconditioning using chemogenetic approach in rats. We demonstrated that disruption of the hippocampus during either preconditioning or test selectively impaired the mediated aversion to A while leaving the direct conditioned aversion to X intact. These findings provide the first evidence that the hippocampus is necessary for unimodal gustatory preconditioning, extending previous demonstrations of hippocampal involvement in polymodal protocols. Our work therefore clarifies the critical role of the hippocampus in forming and retrieving purely gustatory associations to guide behavior, highlighting its function as a central hub for memory integration.</div></div>","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"226 ","pages":"Article 108187"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148308566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trazodone reduces sign-tracking but not goal-tracking in male Sprague Dawley rats","authors":"John Michael Holden,&nbsp;Liam Kubitschek","doi":"10.1016/j.nlm.2026.108185","DOIUrl":"10.1016/j.nlm.2026.108185","url":null,"abstract":"<div><div>Sign-tracking refers to interaction with or approach of an appetitive conditioned stimulus (CS) and is a behavior with implications for cue-induced relapse in those in rehabilitation from drug use. Pharmacological options for reducing sign-tracking may therefore be of use in rehabilitative efforts. Trazodone is a commonly employed antidepressant drug with effects on serotonin, adrenergic and histamine receptors. Previously our laboratory has found that serotonergic antidepressants reduced sign-tracking; as such, we hypothesized that trazodone would reduce aspects of sign-tracking. Male Sprague-Dawley rats were trained in a basic sign-tracking task and were intraperitoneally administered trazodone or vehicle during drug testing. It was shown that trazodone administration significantly reduced sign-tracking probability and total number of responses (the second in sign-trackers only) and increased latency to sign-track, without affecting measures of goal-tracking. Trazodone may have some benefits in reducing sign-tracking and thereby lowering the chance of cue-induced relapse in persons attempting rehabilitation from drug use.</div></div>","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"226 ","pages":"Article 108185"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148278161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"REM sleep fragmentation is associated with impaired configural threat learning","authors":"Bruna Cuccurazzu,&nbsp;Patrick Vizeli,&nbsp;Erin Natale,&nbsp;Cindy Napan,&nbsp;Sean P.A. Drummond,&nbsp;Daniel M. Stout","doi":"10.1016/j.nlm.2026.108183","DOIUrl":"10.1016/j.nlm.2026.108183","url":null,"abstract":"<div><div>Rapid eye movement (REM) phases of sleep are consistently disrupted after trauma and in post-traumatic stress disorder (PTSD). REM disruption impairs cued fear learning, a core element of trauma processing linked to PTSD risk and symptom persistence. Configural threat learning depends on the hippocampus and may be influenced by REM sleep, though its role in humans remains unclear. Here, 55 healthy participants were randomly assigned to REM sleep fragmentation or a control group without sleep disruption for two nights. On the final day, participants completed a configural threat learning task while electrodermal activity (EDA) and behavioral threat expectancy ratings were recorded. REM fragmentation group (REM frag group) had significantly lower threat responses as measured by EDA to the threat configuration relative to the control group. Relative to the REM frag group, the control group showed a significantly greater increase in threat discrimination from the first to the second block of learning. Polysomnography revealed that weighted REM efficiency, but not slow wave sleep or total sleep time, was significantly associated with configural threat learning. REM sleep fragmentation did not affect mnemonic pattern separation, a non-threat measure of hippocampal learning. These results provide evidence that REM sleep is a critical component of configural threat. These findings set the stage for future investigations into how REM sleep disruptions may impair the neural processes supporting threat generalization and discrimination in PTSD, with implications for targeted sleep-based interventions aimed at modulating trauma-related learning and memory.</div></div>","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"226 ","pages":"Article 108183"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148284117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling the coexistence of NMDAR-dependent LTP and LTD mediated by changes in AMPAR conductance","authors":"Berke Ozgur Arslan,&nbsp;Ismail Akturk,&nbsp;Neslihan Serap Sengor,&nbsp;Onur Alpturk","doi":"10.1016/j.nlm.2026.108184","DOIUrl":"10.1016/j.nlm.2026.108184","url":null,"abstract":"<div><div>In this work, we develop a mathematical model that captures both the early and late phases of Long-Term Potentiation (LTP) and Long-Term Depression (LTD), incorporating NMDAR-dependent induction and changes in AMPAR conductance. The model combines multiple essential properties. First, it emphasizes a detailed representation of biochemical processes within the postsynaptic neuron, thereby illustrating the interaction between LTD and distinct forms of LTP. Second, the dynamic modulation of postsynaptic AMPA receptor conductance is represented through nonlinear differential equations and algebraic relations. Third, the model incorporates <em>input specificity</em>, <em>associativity</em>, and <em>cooperativity</em>, allowing synaptic changes at one site to influence the strength of neighboring synapses. These features provide a comprehensive description of synaptic dynamics, allowing the simulation of plasticity at both the cellular and the network levels. Overall, the model offers a valuable framework for studying NMDAR-dependent LTP and LTD by explicitly incorporating changes in AMPAR conductance. We believe that this model provides deeper insights into the molecular mechanisms of synaptic plasticity and paves the way for the construction of network-level models by linking multiple cells through AMPA receptor conductance.</div><div><strong>Significance statement</strong>: We present a comprehensive mathematical framework that integrates early (E-LTP), late (L-LTP), and LTD by incorporating NMDAR-dependent signaling and changes in AMPAR conductance. By combining and extending established biochemical models, our approach links molecular signaling, receptor trafficking, and postsynaptic membrane dynamics to changes in synaptic strength. The model reproduces key experimental phenomena, including input specificity, associativity, and cooperativity, and clarifies how pathways, such as CaMKII and PKA govern the stability of synaptic modifications. By capturing both cellular- and network-level properties, this framework provides a foundation for building scalable neural models grounded in the biophysics of learning and memory.</div></div>","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"226 ","pages":"Article 108184"},"PeriodicalIF":2.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148302482","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redefining Pavlovian conditioning","authors":"Michael S. Fanselow","doi":"10.1016/j.nlm.2026.108168","DOIUrl":"10.1016/j.nlm.2026.108168","url":null,"abstract":"<div><div>Pavlovian conditioning is typically defined as a form of learning in which a neutral stimulus, through repeated pairing with an unconditional stimulus (US) that elicits an unconditional response (UR), comes to evoke a conditional response (CR) that is related to the UR. I argue that each substantive element of this common definition is empirically and conceptually flawed and that it obscures conditioning’s central role in everyday adaptive behavior. I develop an alternative framework in which Pavlovian conditioning is the process by which organisms learn to recognize biologically significant objects (e.g., foods, mates, predators, toxins) and generate phylogenetically appropriate responses via functional behavior systems organized along imminence continua. Within this view, CSs and USs are features of objects, with the difference that a US serves to tag the object as belonging to a specific behavior system. CRs consist of behavior system mode-specific behaviors and broad changes in reactivity (Pavlovian sensitization). This reconceptualization provides new definitions of CS, US, CR, and UR and situates Pavlovian conditioning as a pervasive mechanism for immediate adaptive action rather than a narrow laboratory phenomenon.</div></div>","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"225 ","pages":"Article 108168"},"PeriodicalIF":1.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147948978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationships between phenotypic differences in punishment behaviour and prefrontal cortex network engagement","authors":"Min Lou,&nbsp;Michelle H. Shen,&nbsp;Saraa Al-Saddik,&nbsp;Luke J. Keevers,&nbsp;Philip Jean-Richard-dit-Bressel","doi":"10.1016/j.nlm.2026.108167","DOIUrl":"10.1016/j.nlm.2026.108167","url":null,"abstract":"<div><div>Avoiding actions with negative consequences is fundamental to adaptive behaviour, yet individuals differ drastically in their tendencies to avoid to punishment. Using a conditioned punishment task in male and female rats, we replicate findings of a bimodal distribution of punishment avoidance, and identify four distinct behavioural phenotypes (Sensitive, Hypersensitive, Insensitive, Generalised) that differed in their punishment avoidance, unpunished reward-seeking, and Pavlovian fear. We examined how these phenotypic differences related to cFos (transcriptional activity marker) across prefrontal cortex (PFC) regions. While region-level cFos differences were minimal, covariance and graph-theoretic analyses revealed three functional PFC networks predominantly composed of medial PFC, ventrolateral PFC, or sensorimotor regions. Activity in the ventrolateral PFC network predicted punishment avoidance, while activity in the medial PFC network predicted generalised suppression during initial punishment learning. These findings suggest phenotypic differences in punishment sensitivity are underpinned by differential recruitment of distinct cortical networks that drive adaptive versus maladaptive responses to negative outcomes.</div></div>","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"225 ","pages":"Article 108167"},"PeriodicalIF":1.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147931914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"On the generality of behavioral theory and abstract phenomena","authors":"Ralph R. Miller","doi":"10.1016/j.nlm.2026.108166","DOIUrl":"10.1016/j.nlm.2026.108166","url":null,"abstract":"<div><div>Pavlov’s research on conditioning, perhaps due to his place in founding the field, was limited to identifying a small number of core principles. This may explain why most of his findings have proven to be of broad generality. A century later, associative learning, including Pavlovian conditioning, is viewed as encompassing a multitude of principles, with most being influenced by a number of independent variables, and we are still far from identifying all the independent variables for each principle. However, it is already clear that many behavioral principles share consequential independent variables, making it difficult to examine any given principle in isolation. This precludes making generalizable predictions, except for further studies in the same laboratory setting where most independent variables can be held constant across experiments. When exported to other laboratories or applied situations, this is usually not feasible. While there is theoretical value in identifying how select independent variables influence behavioral phenomena when other independent variables are held constant, I assert that generalizing the findings to different laboratory settings or applied situations is highly prone to being unsuccessful because these ‘other variables’ will differ from those of the initial laboratory. Nonetheless, academic and funding structures reward researchers who claim great generality concerning behavioral phenomena in the abstract (e.g., ‘blocking’ as the result of simply stated procedures devoid of specific parameters). The central contribution of this paper is to suggest factors that have led behavioral psychology to develop this penchant for claiming broad generality and to advocate for more conceptual replications, so we are less apt to be distracted by phenomena of limited generality.</div></div>","PeriodicalId":19102,"journal":{"name":"Neurobiology of Learning and Memory","volume":"225 ","pages":"Article 108166"},"PeriodicalIF":1.8,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147960138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}