Mol Pain
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Offset analgesia is defined by a dramatic drop in perceived pain intensity with a relatively small decrease in noxious input. Although functional magnetic resonance imaging studies implicate subcortical descending inhibitory circuits during offset analgesia, the role of cortical areas remains unclear. The current study identifies cortical correlates of offset analgesia using functional near infrared spectroscopy (fNIRS). ⋯ These data demonstrate opposing cortical activation patterns during offset analgesia and support a model in which right dlPFC underlies ongoing evaluation of pain intensity change. With predictions of decreasing pain intensity, right dlPFC activation likely inhibits ascending noxious input via subcortical pathways resulting in SSC and mPFC deactivation. This study identifies cortical circuitry underlying offset analgesia and introduces the use of fNIRS to study pain modulation in an outpatient clinical environment.
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Prior studies identified iron deposition in deep brain nuclei and the periaqueductal gray matter region in chronic migraine, and less is known about the cerebral iron deposition over the whole cerebral gray matter in CM. The aim of this case-control study is to investigate the cerebral iron deposition of gray matter in CM using an advanced quantitative susceptibility mapping. ⋯ CM patients had increased iron deposition in total cerebral gray matter which could be considered as a potential diagnostic and evaluated imaging biomarker in CM.
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Thermal nociception involves the transmission of temperature-related noxious information from the periphery to the CNS and is a heritable trait that could predict transition to persistent pain. Rodent forward genetics complement human studies by controlling genetic complexity and environmental factors, analysis of end point tissue, and validation of variants on appropriate genetic backgrounds. Reduced complexity crosses between nearly identical inbred substrains with robust trait differences can greatly facilitate unbiased discovery of novel genes and variants. ⋯ Whole brain proteomics further supported decreased H2AFY expression could underlie enhanced hot plate sensitivity, and identified ACADS as a candidate for reduced brain weight. To summarize, a BALB/c reduced complexity cross combined with multiple-omics approaches facilitated identification of candidate genes underlying thermal nociception and brain weight. These substrains provide a powerful, reciprocal platform for future validation of candidate variants.
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In the mid-1990s, the development of combination antiretroviral therapy converted HIV infection into a chronic condition, with newly diagnosed patients now living longer than the general population. HIV affects both the central and peripheral nerve systems, resulting in a variety of clinical problems, including peripheral neuropathy, which is a common neurological consequence. Despite this, there is a scarcity of data on the extent of peripheral sensory neuropathy and its underlying factors in Ethiopia, necessitating this study. ⋯ Peripheral sensory neuropathy was incredibly common. Accordingly, peripheral sensory neuropathy was found considerably associated with age, viral load level, stage of the disease, and DM comorbidity. It is vital to integrate routine peripheral sensory neuropathy screening strategies for clients who are on ART follow up for prevention and early identification of the problem.
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Oxytocin (OT) is recognized as a critical neuropeptide in pain-related disorders. Chronic pain caused by the comorbidity of temporomandibular disorder (TMD) and fibromyalgia syndrome (FMS) is common, but whether OT plays an analgesic role in the comorbidity of TMD and FMS is unknown. Female rats with masseter muscle inflammation combined with 3-day forced swim (FS) stress developed somatic hypersensitivity, which modeled the comorbidity of TMD and FMS. ⋯ The expression of OT receptors and 5-HT2A receptors in the L4-L5 spinal dorsal horn significantly increased following intrathecal injection of 0.5 μg OT. Intrathecal administration of either the OT receptor antagonist atosiban or 5-HT2A receptor antagonist ritanserin blocked the analgesic effect of OT. These results suggest that OT may inhibit hindpaw hyperalgesia evoked by orofacial inflammation combined with stress through OT receptors and/or 5-HT2A receptors, thus providing a therapeutic prospect for drugs targeting the OT system and for patients with comorbidity of TMD and FMS.