Sepsis-induced encephalopathy impairs descending nociceptive pathways in rats

Abstract

Sepsis-associated encephalopathy (SAE) is a significant problem in patients with sepsis, and it is associated with a decrease in cognitive and sensitivity capability induced by systemic inflammation. SAE is implicated in reversible brain damage of several regions related to cognition, emotion, and sensation; however, it is not well established if it could affect brain regions associated with nociceptive modulation. Here were evaluated the nociceptive thresholds in rats with systemic inflammation induced by cecal ligation puncture (CLP). After 24 h of CLP, it was observed an increase in nociceptive threshold in all tests. Periaqueductal gray, rostroventral medulla, critical regions for descending nociceptive modulation, were evaluated and showed enhanced pro-inflammatory cytokines as well as glial activation. These results suggest that systemic inflammation could compromise descending facilitatory pathways, impairing nociceptive sensory functioning.

Fisetin ameliorates cognitive impairment by activating mitophagy and suppressing neuroinflammation in rats with sepsis‐associated encephalopathy

“… 22 Based on recent studies, many brain areas, including the cortex, thalamus, hippocampus, striatum, basal ganglia, and corpus callosum could be affected by CLP. 23 , 24 , 25 Of note, the hippocampus region has a close association with cognitive impairment, 26 so the hippocampus tissue was selected for our research. As demonstrated in this study, septic rats showed significant cognitive deficits, including prolonged escape latency, increased escape passage, reduced frequency of cross to the platform, and enlarged neuronal apoptosis.…”

“…Sepsis is a common but lethal cause for multiple organ dysfunction, and SAE is the pathological change when septic damages spread to the brain, characterized by diffused brain dysfunction 22 . Based on recent studies, many brain areas, including the cortex, thalamus, hippocampus, striatum, basal ganglia, and corpus callosum could be affected by CLP 23–25 . Of note, the hippocampus region has a close association with cognitive impairment, 26 so the hippocampus tissue was selected for our research.…”

Self-Reported Pain and Pain Observations in People with Korsakoff’s Syndrome: A Pilot Study

“…However, the lateral pain system is particularly involved in the sensorydiscriminative features of pain such as the recognition of location, intensity, and nature of nociceptive stimuli (e.g., sharp or dull) [14]. It is still unknown which parts of these pain systems are involved in KS, but it has been confirmed in rodents that the periaqueductal gray, cerebellar, and cerebral cortices are involved in increased pain thresholds [11,15,16]. Since these brain areas are also impaired in people with KS, it could be that there might also be higher pain thresholds in KS [11].…”

Canabidiol em modelo pré-clínico de dor neuropática: uma avaliação dos aspectos sensoriais, emocionais e inflamatórios relacionados com a modulação da sensibilidade dolorosa

“…O sobrenadante dos tecidos processados foi usado para quantificação de proteínas e citocinas. A concentração de proteína tecidual total foi medida pelo kit de ensaio de proteína BCA (Pierce)(Cazuza et al, 2020). Os níveis de citocinas IL1-β, IL-6 e IL-10 foram determinados usando kits ELISA apropriados (R&D Systems, Minneapolis,2.11.…”