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Aims: The mechanism underlying postoperative post-traumatic stress disorder (PTSD) remains unclear. However, studies have shown that acute postoperative pain is an independent risk factor for PTSD, which is also closely related to memory consolidation enhancement. Preoperative patients often experience unpleasant traumatic events, and postoperative pain usually occurs in the memory consolidation stage of these events. Therefore, inquiring whether acute postoperative pain affects memory consolidation and its possible mechanism may help to explain the causes of postoperative PTSD.
Methods And Results: In this study, we show that the surgical incision pain enhances the consolidation of emotional memory (in the passive avoidance test) and nonemotional memory (in the novel object recognition test) in mice. None of the behaviors evaluated were affected by anxiety or locomotor dysfunction (in the open-field test). Besides, we confirmed that surgical incision pain promotes memory enhancement by enhancing memory consolidation instead of memory retrieval. Furthermore, the consolidation of emotional memory and nonemotional memory was enhanced by the activation of the LC-HPC TH projection after surgical incision pain. Hippocampal CA1 dopamine receptors, rather than β adrenoceptors, mediate emotional and nonemotional memory consolidation enhancement after surgical incision pain.
Conclusion: Thus, our results indicate that surgical incision pain enhances the memory consolidation of emotional memory and nonemotional memory in mice. Activation of the LC-HPC TH projection may contribute to memory consolidation enhancement induced by surgical incision pain, which involves the activity of dopamine receptors in CA1.
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http://dx.doi.org/10.1111/cns.70570 | DOI Listing |
J Neurochem
September 2025
Astbury Centre for Structural Molecular Biology, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
Memory formation involves a complex interplay of molecular and cellular processes, including synaptic plasticity mechanisms such as long-term potentiation (LTP) and long-term depression (LTD). These processes rely on activity-dependent gene expression and local protein synthesis at synapses. A central unresolved question in neuroscience is how memories can be stably maintained over time, despite the transient nature of the proteins involved in their initial encoding.
View Article and Find Full Text PDFNeuropsychologia
September 2025
Department of Experimental Psychology and Oxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford, United-Kingdom. Electronic address:
Models of memory consolidation propose that newly acquired memory traces undergo reorganisation during sleep. To test this idea, we recorded high-density electroencephalography (EEG) during an evening session of word-image learning followed by immediate (pre-sleep) and delayed (post-sleep) recall. Polysomnography was employed throughout the intervening night, capturing time spent in different sleep stages.
View Article and Find Full Text PDFNeuropsychologia
September 2025
University of Adelaide, Adelaide, South Australia, Australia 5000.
Sleep neurophysiology undergoes significant changes across the lifespan, which coincide with age-related differences in memory, particularly for emotional information. However, the mechanisms that underlie these effects remain poorly understood. One potential mechanism is the aperiodic component, which reflects "neural noise", differs across age, and is predictive of perceptual and cognitive processes.
View Article and Find Full Text PDFSince Freud, psychologists have sought to decipher the language of dreams, but no universal interpretive manual exists. Advances in dream neuroscience and the emergence of Code Biology have brought us closer to understanding the rules and functions underlying dream formation. Code Biology, which studies coding processes in living systems, offers a revolutionary framework for how neural and symbolic patterns generate dream narratives.
View Article and Find Full Text PDFStudy Objectives: Brief sleep loss alters cognition and the activity and synaptic structures of both principal neurons and interneurons in hippocampus. However, although sleep-dependent coordination of activity between hippocampus and neocortex is essential for memory consolidation, much less is known about how sleep loss affects neocortical input to hippocampus, or excitatory-inhibitory balance within neocortical structures. We aimed to test how the synaptic structures of SST+ interneurons in lateral and medial entorhinal cortex (LEC and MEC), which are the major neocortical input to hippocampus, are affected by brief sleep disruption in the hours following learning.
View Article and Find Full Text PDF