Sleep and physical activity are modifiable behaviours linked to pain. Sleep disturbance often co-occurs with persistent pain and may contribute to its development. Exercise is a first-line treatment f Show more
Sleep and physical activity are modifiable behaviours linked to pain. Sleep disturbance often co-occurs with persistent pain and may contribute to its development. Exercise is a first-line treatment for chronic pain. Previous work showed that sleep disturbance worsens and prolongs postinjury pain behaviours, exercise mitigates these effects, and brain-derived neurotrophic factor may play a mechanistic role. Deeper insight requires a broader assessment of pain behaviours and systemic biomarkers related to inflammation, tissue repair, and neuromodulation. This study addresses these gaps. Twenty-nine adult female Sprague-Dawley rats performed an intensive lever-pulling task for 4 weeks to induce overuse injury and then underwent one of three 4-week interventions: intermittent sleep disturbance, voluntary exercise (via access to a running wheel), or both. Pain-related behaviours and 71 blood analytes were measured immediately preinjury, postinjury, and postintervention. Overuse injury decreased grip strength and increased mechanical sensitivity in the injured forepaws. After cessation of the injury inducing task, these changes persisted with sleep disturbance but recovered to, or exceeded, preinjury levels with exercise, even with concurrent sleep disturbance. Biomarker analyses revealed distinct neuroimmune responses to injury and sleep disturbance, particularly mediators of inflammation and neuroplasticity, that were offset by exercise. Correlations between biomarkers and behavioural outcomes support mechanistic links between injury, sleep, exercise, and recovery. Findings demonstrate that postinjury sleep disturbance induces neuroimmune changes that increase persistent pain vulnerability, whereas aerobic exercise counters these effects. This highlights the interaction between sleep and exercise in recovery and their potential as strategies to prevent and manage chronic pain. Show less
This research investigated the potential therapeutic role of α-(phenylselanyl) acetophenone (PSAP) in the comorbidity of chronic pain and depression triggered by partial sciatic nerve ligation (PSNL). Show more
This research investigated the potential therapeutic role of α-(phenylselanyl) acetophenone (PSAP) in the comorbidity of chronic pain and depression triggered by partial sciatic nerve ligation (PSNL). Male Swiss mice underwent PSNL surgery, and after a four-week period, they received either PSAP (1-50 mg/kg, administered intragastrically) or imipramine (IMI) (50 mg/kg) 30 min prior to behavioral assessments. Both PSAP and IMI effectively alleviated PSNL-induced hypersensitivity to pain and depressive-like symptoms, as demonstrated in forced swim and allodynia tests. Additionally, PSAP counteracted the elevated levels of lipid peroxidation and reactive oxygen species observed in the cortex and hippocampus following PSNL. These neuroprotective effects appear to be linked to PSAP's anti-inflammatory properties, as it downregulated the expression of pro-inflammatory markers such as NF-κB p65, TNF-α, and IDO mRNA in the affected brain regions. Furthermore, PSAP restored hippocampal BDNF mRNA levels, which had been diminished by nerve injury. Since inflammation is a common pathway in both chronic pain and depression, the findings indicate that PSAP holds promise as a treatment for this comorbid condition. Show less