ArticleCNS neuroscience & therapeutics2023
Hippocampus-prefrontal cortex inputs modulate spatial learning and memory in a mouse model of sepsis induced by cecal ligation puncture.
Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Current knowledge and challenges of sepsis-associated encephalopathy.Intensive care medicine · 2026Review
- Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026Review
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Short-chain fatty acids attenuate sepsis-induced gut dysbiosis and hippocampal neuroinflammation via NLRP6 inflammasome activation in mice.International journal of surgery (London, England) · 2026Article
- Protective Effects of Fish Oil Against Brain Impairment in Rats with Chronic Ethanol-Induced Liver Damage Involving the NRF2 Pathway and Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Article
- Lactate-induced macrophage HMGB1 lactylation promotes neutrophil extracellular trap formation in sepsis-associated acute kidney injury.Cell biology and toxicology · 2025Article
- Editome profiling and cross-cohort validation reveal A-to-I RNA editing dysregulation in the hippocampus and prefrontal cortex of sepsis patients.Frontiers in psychiatry · 2025Article
- Study on the predictive value of early microcirculation perfusion indicators combined with neuroelectrophysiological monitoring for the occurrence and prognosis of sepsis-associated encephalopathy in neurocritical care patients.Frontiers in neurology · 2025Article
- Nogo-A exacerbates sepsis-associated encephalopathy by modulating microglial SHP-2/NLRP3 balance and inducing ROS and M1 polarization.Biomolecules & biomedicine · 2024Article
- Article
- RIPK3 activation promotes DAXX-dependent neuronal necroptosis after intracerebral hemorrhage in mice.CNS neuroscience & therapeutics · 2024Article
- The role of the peripheral system dysfunction in the pathogenesis of sepsis-associated encephalopathy.Frontiers in microbiology · 2024Review
- Hippocampal adenosine-to-inosine RNA editing in sepsis: dynamic changes and influencing factors.Brain communications · 2024Article
- TRIM45 aggravates microglia pyroptosis via Atg5/NLRP3 axis in septic encephalopathy.Journal of neuroinflammation · 2023Article
- Corticosterone enhances formation of non-fear but not fear memory during infectious illness.Frontiers in behavioral neuroscience · 2023Article
- Peripheral inflammation and neurocognitive impairment: correlations, underlying mechanisms, and therapeutic implications.Frontiers in aging neuroscience · 2023Review
- Hippocampus-prefrontal cortex inputs modulate spatial learning and memory in a mouse model of sepsis induced by cecal ligation puncture.CNS neuroscience & therapeutics · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsSepsis-associated encephalopathy (SAE) often leads to cognitive impairments. However, the pathophysiology of SAE is complex and unclear. Here, we investigated the role of hippocampus (HPC)-prefrontal cortex (PFC) in cognitive dysfunction in sepsis induced by cecal ligation puncture (CLP) in mice.
methodsThe neural projections from the HPC to PFC were first identified via retrograde tracing and viral expression. Chemogenetic activation of the HPC-PFC pathway was shown via immunofluorescent staining of c-Fos-positive neurons in PFC. Morris Water Maze (MWM) and Barnes maze (BM) were used to evaluate cognitive function. Western blotting analysis was used to determine the expression of glutamate receptors and related molecules in PFC and HPC.
resultsChemogenetic activation of the HPC-PFC pathway enhanced cognitive dysfunction in CLP-induced septic mice. Glutamate receptors mediated the effects of HPC-PFC pathway activation in CLP mice. The activation of the HPC-PFC pathway resulted in significantly increased levels of NMDAR, AMPAR, and downstream signaling molecules including CaMKIIa, pCREB, and BDNF in PFC. However, inhibition of glutamate receptors using 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo (F)quinoxaline (NBQX), which is an α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR inhibitor), or D-2-amino-5-phosphonopentanoate (D-AP5), which is an NMDA receptor antagonist abolished this increase.
conclusionOur study reveals the important role of the HPC-PFC pathway in improving cognitive dysfunction in a mouse model of CLP sepsis and provides a novel pathogenetic mechanism for SAE.
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