Abstract
Neuropathic pain induced by a nerve injury can lead to chronic pain. Recent studies have reported hyperactive neural activities in the nociceptive-related area of the brain as a result of chronic pain. Although cerebral activities associated with hyperalgesia and allodynia in chronic pain models are difficult to represent with functional imaging techniques, advances in manganese (Mn)-enhanced magnetic resonance imaging (MEMRI) could facilitate the visualization of the activation of pain-specific neural responses in the cerebral cortex. In order to investigate the alleviation of pain nociception by mammalian target of rapamycin (mTOR) modulation, we observed cerebrocortical excitability changes and compared regional Mn2+ enhancement after mTOR inhibition. At day 7 after nerve injury, drugs were applied into the intracortical area, and drug (Vehicle, Torin1, and XL388) effects were compared within groups using MEMRI. Therein, signal intensities of the insular cortex (IC), primary somatosensory cortex of the hind limb region, motor cortex 1/2, and anterior cingulate cortex regions were significantly reduced after application of mTOR inhibitors (Torin1 and XL388). Furthermore, rostral-caudal analysis of the IC indicated that the rostral region of the IC was more strongly associated with pain perception than the caudal region. Our data suggest that MEMRI can depict pain-related signal changes in the brain and that mTOR inhibition is closely correlated with pain modulation in chronic pain rats.
Highlights
Neuropathic pain arises from an initial injury, such as neuropathy caused by a lesion of or damage to the somatosensory nervous system, that can lead to chronic pain [1]
With manganese-enhanced magnetic resonance imaging (MEMRI) studies having been found useful in identifying pain pathways in the brain, various pain imaging studies have been performed in the spinal cord and brain [5, 6], allowing researchers to visualize nerve injury [10] and thermal [11] stimulus-induced abnormal brain activities
The purpose of this study was to evaluate the usefulness of MEMRI in chronic pain research using whole brain analysis, as well as to measure changes in brain activities after drug administration in a chronic pain model
Summary
Neuropathic pain arises from an initial injury, such as neuropathy caused by a lesion of or damage to the somatosensory nervous system, that can lead to chronic pain [1]. While identifying brain abnormalities underlying chronic pain sensation could be a first step in clinical treatment, investigation of changes in cerebral neuronal activity is a challenge for functional imaging. Experimental hyperalgesia produces the upregulated neuronal activation of brain responses within pain-processing regions, including the anterior cingulate cortex (ACC), insular cortex (IC), and primary (SI) and secondary somatosensory cortices (SII) [7,8,9]. With MEMRI studies having been found useful in identifying pain pathways in the brain, various pain imaging studies have been performed in the spinal cord and brain [5, 6], allowing researchers to visualize nerve injury [10] and thermal [11] stimulus-induced abnormal brain activities. Our previous formalin-induced pain study showed that MEMRI could be a good indicator of paininduced changes in the central nervous system (CNS)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
