ArticleCNS neuroscience & therapeutics2024
Serotonergic neurotransmission mediated cognitive dysfunction in two mouse models of sepsis-associated encephalopathy.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026Review
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Circulating adipocyte fatty acid-binding protein exacerbates LPS-induced neurotoxicity by crossing the disrupted blood-brain barrier and promoting neuronal apoptosis.Cell communication and signaling : CCS · 2026Article
- 5-Hydroxytryptophan, a Precursor for Serotonin Synthesis, Alleviated Cognitive Dysfunction in a Mouse Model of Sepsis-Associated Encephalopathy.Biomedicines · 2025Article
- Loss of M1 Acetylcholine Receptor-mediated Orexinergic Activity Contributes to Immune Dysfunction in Experimental Sepsis.Research square · 2025Article
- The progress of the microbe-gut-brain axis in sepsis-associated encephalopathy.Frontiers in cellular and infection microbiology · 2025Review
- Gut microbiota and sepsis-associated encephalopathy: pathogenesis and precision therapies.Frontiers in neuroscience · 2025Review
- Protective Effects of Mdivi-1 on Cognition Disturbance Following Sepsis in Mice via Alleviating Microglia Activation and Polarization.CNS neuroscience & therapeutics · 2025Article
- Serotonergic neurotransmission mediated cognitive dysfunction in two mouse models of sepsis-associated encephalopathy.CNS neuroscience & therapeutics · 2024Article
- The multifaceted effects of fluoxetine treatment on cognitive functions.Frontiers in pharmacology · 2024Review
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundPatients with sepsis-associated encephalopathy (SAE) often exhibit cognitive impairments. Despite this, the underlying mechanisms of SAE remain largely unexplored. Here, we explored the role of serotonergic neurotransmission in cognitive dysfunction of two mouse models of SAE.
methodsThe mouse models of SAE were established by injection of lipopolysaccharide (LPS, 10 mg/kg, intraperitoneal) and cecal ligation puncture (CLP) respectively. Barnes maze, new object recognition test and open field test were used to evaluate the effects of fluoxetine (selective serotonin reuptake inhibitor) and cyproheptadine (nonselective 5-HT
resultsBoth LPS-induced sepsis and CLP induced sepsis resulted in a notable learning deficit. Fluoxetine ameliorated, while cyproheptadine aggravated, cognitive impairment in two classic mouse models of SAE. The cognition-enhancing effect of fluoxetine is reversed by WAY100635. Decreased 5-HT levels in hippocampus, brainstem and frontal lobe were observed in LPS septic model and CLP septic model. Notably, both fluoxetine and cyproheptadine significantly increased 5-HT levels in those brain regions in LPS septic model. Additionally, fluoxetine significantly increased 5-HT levels in frontal lobe of CLP septic model.
conclusionsOur study demonstrated that serotonergic neurotransmission plays a significant role in mechanisms underlying cognitive impairment in SAE. These findings contribute to identification of novel targets to prevent and arrest cognitive impairment in SAE.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.