Pain
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Spatial summation (SS) and spatial discrimination (SD) are essential for pain perception. In the cold-pain sensation, these processes have hardly been studied. Our aim was to study the SS and SD of cold pain, as well as the SS of cold-pain threshold (CPT) in hairy and glabrous skin. ⋯ CPT was significantly higher in hairy than glabrous skin, but the amount of SS of CPT was similar in the 2 skin types. Noxious cold-evoked thermal qualities were more common in the glabrous than the hairy skin. In conclusion: (1) SS and SD of cold pain are reciprocal; (2) whereas cold pain can summate over large distances, the SD of cold pain is poor; (3) SS of cold pain does not exist between contralateral body sides, however, inhibition occurs; (4) SS is independent of skin type and sensitivity to cold pain; (5) differences in pain quality between hairy and glabrous skin may reflect innervation differences.
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This study assessed functional brain activation in rats during expectation of visceral pain. Male rats were trained in step-down passive avoidance (PA) for 2 days. Upon stepping down from a platform, conditioned animals received noxious colorectal distension delivered through a colorectal balloon, whereas the balloon in control rats remained uninflated. ⋯ The amygdala and cerebellar hemispheres formed another positively connected cluster, which was negatively connected with the corticostriatal cluster, suggesting corticolimbic modulation. Prelimbic cortex, nucleus accumbens, and anterior insula emerged in conditioned animals as hubs. Our results show that during retrieval of PA, brain areas implicated in PA expression as well as those implicated in acute visceral pain processing were recruited, in line with findings from human brain imaging studies on pain expectation.
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Persistent pain after resolution of clinically appreciable signs of arthritis poses a therapeutic challenge, and immunosuppressive therapies do not meet this medical need. To investigate this conversion to persistent pain, we utilized the K/BxN serum transfer arthritis model, which has persistent mechanical hypersensitivity despite the resolution of visible inflammation. Toll-like receptor (TLR) 4 has been implicated as a potential therapeutic target in neuropathic and other pain models. ⋯ WT arthritic mice had reduced spinal levels of the anti-inflammatory prostaglandin 15-deoxy-Δ(12,14)-PGJ(2) (15d-PGJ(2)) on day 6, compared to IT LPS-RS-treated mice. Direct IT application of 15d-PGJ(2) (0.5 μg) on day 6 improved mechanical hypersensitivity in arthritic mice within 15 min. Hence, TLR4 signaling altered spinal bioactive lipid profiles in the serum transfer model and played a critical role in the transition from acute to chronic postinflammatory mechanical hypersensitivity.
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Complex regional pain syndrome (CRPS) is a painful condition affecting one or more extremities of the body, marked by a wide variety of symptoms and signs that are often difficult to manage because the pathophysiology is incompletely understood. Thus, diverse treatments might be ineffective. A recent report revealed the presence of autoantibodies against differentiated autonomic neurons in CRPS patients. ⋯ We identified these autoantibodies as immunoglobulin G directed against peptide sequences from the second extracellular loop of these receptors. The identification of functionally active autoantibodies in serum samples from CRPS patients supports an autoimmune pathogenesis of CRPS. Thus, our findings contribute to the further understanding of this disease, could help in the diagnosis in future, and encourage new treatment strategies focusing on the immune system.
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Cutaneous inflammation induced by ultraviolet (UV) irradiation in the UV-B range has received significant recent interest as a translational inflammatory pain model. Changes in thermal and mechanical sensitivities in the area of primary hyperalgesia are well documented in both the rat and human UV-B models, but the occurrence of secondary mechanical hyperalgesia is controversial. We investigated the occurrence of secondary mechanical hyperalgesia in the rat UV-B model. ⋯ Heat rekindling also induced a significant mechanical hyperalgesia and allodynia on the contralateral hind paw, further suggesting the contribution of central sensitisation. Our data provide strong evidence for a central contribution in both the rat UV-B pain model and an enhanced contribution in the new model combining UV-B irradiation with heat rekindling. We also elucidate potential differences in the methods used by ourselves and others to obtain mechanical withdrawal thresholds in rats, which may explain the lack of secondary hyperalgesia in the rat UV-B model.