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Postoperative cognitive dysfunction (POCD) is a common postoperative neurological complication, with memory consolidation deficits being one of its prominent features. However, the mechanisms underlying postoperative memory consolidation deficits are still unclear. The perineuronal net (PNN) is a specialized extracellular matrix that predominantly surrounds parvalbumin (PV) interneurons and is closely associated with cognitive functions, including learning and memory. Theta oscillations in the hippocampal CA1 region are crucial for memory consolidation. However, the relationships among postoperative memory consolidation deficits, theta oscillation abnormalities, and PNNs remain unclear. The aim of this study was to investigate the role of PNNs in the CA1 region in postoperative memory consolidation deficits and theta oscillation abnormalities. The experiments revealed that, after anesthesia and surgery, the mice exhibited memory consolidation deficits, abnormal theta oscillations, and PNNs loss in the hippocampal CA1 region. Increasing the density of PNNs alleviated postoperative memory consolidation deficits and theta oscillation abnormalities. In contrast, normal mice treated with chondroitinase ABC (ChABC) to degrade PNNs presented a similar phenotype of postoperative memory consolidation deficits. Further investigations revealed that PNNs loss in surgical mice weakened the inhibitory function of PV interneurons. Increase the density of PNNs reversed these changes, while ChABC degradation of PNNs also weakened the inhibitory function of PV interneurons. Notably, PNNs loss after surgery was associated with increased microglial phagocytosis. In conclusion, the PNNs loss caused by increased microglial phagocytosis in the hippocampal CA1 region after surgery palys an important role in postoperative memory consolidation deficits and theta oscillation abnormalities, which is associated with the impaired function of PV interneurons. This study provides new theoretical insights and potential targets for preventing and treating postoperative memory consolidation deficits.
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http://dx.doi.org/10.1016/j.brainresbull.2025.111433 | DOI Listing |
Endocr Connect
September 2025
Centre for Higher Education Development, University of Cape Town.
Background: Cortisol and growth hormone are important for sleep regulation and cognition. Sleep is critical for cognitive functioning, and memory consolidation. Patients with pituitary disease experience hormonal dysregulation, impaired sleep quality, and cognitive dysfunction.
View Article and Find Full Text PDFJ Psychopharmacol
September 2025
Florey Institute of Neuroscience and Mental Health, Parkville, VIC, Australia.
Rapid eye movement sleep (REMS) has historically been associated with anecdotal 'creative insights', possibly due to the fantastical and ostensibly illuminating nature of its associated phenomena (dreams). REMS, characterised by rapid eye movements, muscle atonia, and high-energy neuronal activity, has been linked to memory consolidation and information processing, particularly regarding the formation of novel associations or reintegration of consolidated memories into new cognitive networks. However, studies in these domains have largely used methodology which deprived subjects (animal or human) of REMS, rather than enhanced it.
View Article and Find Full Text PDFDev Psychobiol
September 2025
Department of Psychology and Center for Neuroscience and Behavior, Miami University, Oxford, Ohio, USA.
Social buffering may reduce the persistent impacts of acute early life stress (aELS) and, thus, has important implications for anxiety- and trauma-related disorders. First, we assessed whether aELS would induce maladaptive fear incubation in adult mice, a PTSD-like phenotype. Overall, animals showed incubation of fear memory in adulthood, independent of aELS condition.
View Article and Find Full Text PDFJ 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.
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