Articles: hyperalgesia.
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Complex regional pain syndrome (CRPS) is not a very common yet typical complication of extremity trauma in the daily practice of a trauma surgeon. The pathophysiology of this puzzling disease is still not completely understood and its impact on the patient cannot be overestimated. ⋯ While a multitude of different diagnostic systems has led to confusion in the past, we now have an internationally accepted, validated and easy to reproduce diagnostic algorithm in the form of the Budapest criteria. The adequate therapy is still a field for debate, but there is now a broad choice of conservative and interventional treatments for the out- and inpatient setting.
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Sickle cell disease (SCD) is a genetic blood disorder that impacts millions of individuals worldwide. SCD is characterized by debilitating pain that can begin during infancy and may continue to increase throughout life. This pain can be both acute and chronic. ⋯ Thus, pain management in SCD remains a major challenge. Humanized transgenic mice expressing exclusively human sickle hemoglobin show features of pain and pathobiology similar to that in patients with SCD. Therefore, these mice offer the potential for investigating the mechanisms of pain in SCD and allow for development of novel targeted analgesic therapies. © 2018 by John Wiley & Sons, Inc.
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Neuroscience letters · Sep 2018
The left central nucleus of the amygdala contributes to mechanical allodynia and hyperalgesia following right-sided peripheral nerve injury.
The left and right central nucleus of the amygdala (CeA) exert asymmetric pronociceptive functions. In the setting of a transient noxious stimulus or persistent inflammatory pain, neuronal activity increases in the right but not left CeA, regardless of side of injury. Much less is known regarding this lateralization with respect to the behavioral manifestations of persistent neuropathic pain. ⋯ Following right-sided SNI, we observed a modality-dependent effect: mechanical allodynia was attenuated by inactivation of the left but neither the right nor bilateral CeA, mechanical hyperalgesia was attenuated by left, right and bilateral intra-CeA lidocaine, and cold allodynia was unaffected. These data suggest that CeA-mediated control of neuropathic pain is not strictly limited to the right CeA as previously assumed. We conclude that functional lateralization depends on the type of pain, side of injury and the sensory modality, and that the left CeA contributes to mechanical allodynia and hyperalgesia after peripheral nerve injury to the right side of the body.
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Neuroligin 1 (NLGN1), a cell adhesion molecule present at excitatory glutamatergic synapses, has been shown to be critical for synaptic specialization and N-methyl-d-aspartate (NMDA)-subtype glutamate receptor-dependent synaptic plasticity. Whether and how NLGN1 is engaged in nociceptive behavioral sensitization remains largely unknown. In this study, we found an activity-dependent regulation of NLGN1 synaptic expression in pain-related spinal cord dorsal horns of mice. ⋯ We also found that one of the important roles of NLGN1 was to facilitate the clustering of NMDAR at synapses. The NLGN1-targeting siRNA suppressed the synaptic expression of GluN2B-containing NMDAR in CFA-injected mice and meanwhile, attenuated the inflammatory mechanical allodynia and thermal hypersensitivity. These data suggested that tissue injury-induced synaptic redistribution of NLGN1 was involved in the development of pain hypersensitivity through facilitating the synaptic incorporation of NMDARs.
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Microglia-neuron signalling in the spinal cord is a key mediator of mechanical allodynia caused by peripheral nerve injury. We recently reported sex differences in microglia in pain signalling in mice: spinal mechanisms underlying nerve injury-induced allodynia are microglial dependent in male but not female mice. Whether this sex difference in pain hypersensitivity mechanisms is conserved in other species is unknown. ⋯ Furthermore, chromatin immunoprecipitation-qPCR revealed that the transcription factor IRF5 differentially binds to the P2rx4 promoter region in female rats vs male rats. Finally, mechanical allodynia was produced in otherwise naive rats by intrathecally administering P2X4R-stimulated microglia from male rats but not those from female rats. Together, our findings demonstrate the existence of sexually dimorphic pain signalling in rats, suggesting that this sex difference is evolutionarily conserved, at least across rodent species.