Abstract
Human brain imaging studies have revealed several regions that are activated in patients with chronic pain. In rodent brains, functional changes due to chronic pain have not been fully elucidated, as brain imaging techniques such as functional magnetic resonance imaging and positron emission tomography (PET) require the use of anesthesia to suppress movement. Consequently, conclusions derived from existing imaging studies in rodents may not accurately reflect brain activity under awake conditions. In this study, we used quantitative activation-induced manganese-enhanced magnetic resonance imaging to directly capture the previous brain activity of awake mice. We also observed and quantified the brain activity of the spared nerve injury (SNI) neuropathic pain model during awake conditions. SNI-operated mice exhibited a robust decrease of mechanical nociceptive threshold 14 days after nerve injury. Imaging on SNI-operated mice revealed increased neural activity in the limbic system and secondary somatosensory, sensory-motor, piriform, and insular cortex. We present the first study demonstrating a direct measurement of awake neural activity in a neuropathic pain mouse model.
Highlights
Chronic pain sensitizes against somatosensory stimuli and induces anxiety and depression in patients (Sah et al, 2003)
To elucidate the activated brain regions in neuropathic pain, qAIM-MRI was conducted on spared nerve injury (SNI) and sham-operated groups of mice
The regions showing significant T1 shortening were observed in the secondary somatosensory cortex (S2), sensory-motor cortex (S1, M1, and M2), and piriform cortex (Pir), and insular cortex (IC) (Figure 3)
Summary
Chronic pain sensitizes against somatosensory stimuli and induces anxiety and depression in patients (Sah et al, 2003). These physical and psychological changes are caused by chronic alterations in brain activity. Neuropathic pain is caused by abnormal neural excitation elicited by conditions such as nerve injury, diabetes mellitus, herpes simplex virus infection, and human immunodeficiency virus infection. Since neuropathic pain is resistant against many analgesics including opioids, there are very few therapeutic options. It is established that neuropathic pain results in neuroplasticity that can be observed in several brain regions (Jaggi and Singh, 2011)
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