Articles: hyperalgesia.
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Sensory nerve fibers differ not only with respect to their sensory modalities and conduction velocities, but also in their relative roles for pain hypersensitivity. It is presently largely unknown which types of sensory afferents contribute to various forms of neuropathic and inflammatory pain hypersensitivity. Vesicular glutamate transporter 3-positive (VGluT3(+)) primary afferents, for example, have been implicated in mechanical hypersensitivity after inflammation, but their role in neuropathic pain remains under debate. ⋯ Further, we provide direct evidence that, despite not mediating painful stimuli in naive mice, activation of VGluT3(+) sensory fibers by light elicits pain behavior in the oxaliplatin but not the CCI model. Immunohistochemical and electrophysiological data support a role of transient receptor potential melastatin 8-mediated facilitation of synaptic strength at the level of the dorsal horn as an underlying mechanism. Together, we demonstrate that VGluT3(+) fibers contribute in an etiology-dependent manner to the development of mechano-cold hypersensitivity.
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Acta Anaesthesiol Scand · Sep 2014
Controlled Clinical TrialAssessment of deep tissue hyperalgesia in the groin - a method comparison of electrical vs. pressure stimulation.
Deep pain complaints are more frequent than cutaneous in post-surgical patients, and a prevalent finding in quantitative sensory testing studies. However, the preferred assessment method - pressure algometry - is indirect and tissue unspecific, hindering advances in treatment and preventive strategies. Thus, there is a need for development of methods with direct stimulation of suspected hyperalgesic tissues to identify the peripheral origin of nociceptive input. ⋯ The presented tissue-specific direct deep tissue electrical stimulation technique has equal or superior reliability compared with the indirect tissue-unspecific stimulation by pressure algometry. This method may facilitate advances in mechanism based preventive and treatment strategies in acute and chronic post-surgical pain states.
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Peripheral nerve injury increases the excitability of primary sensory neurons. This triggers the onset of neuropathic pain and maintains its persistence. Because changes in hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels are implicated in this process, we examined the action of the heart-rate-reducing agent, ivabradine, a clinically approved HCN blocker, in the rat chronic constriction injury (CCI) model of neuropathic pain. ⋯ Because ivabradine is effective at an oral dose that produces only moderate pharmacological heart rate reduction, and this is known to be well tolerated in a clinical context, these results underline its possible use in neuropathic pain management.
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Inhibition of Src-family protein tyrosine kinases (SFKs) in spinal dorsal horn has been established as an effective strategy for the alleviation of chronic pathological pain. As one of the important SFKs members, Fyn kinase is critical for synaptic plasticity and many pathophysiological processes. However, whether Fyn is involved in spinal sensitization is far from being elucidated. ⋯ Fyn played a key role in the sustained sensitization of nociceptive behaviours by up-regulating the functions of ionotropic glutamate receptors in spinal dorsal horn.
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The UVB and heat rekindling (UVB/HR) model shows potential as a translatable inflammatory pain model. However, the occurrence of central sensitization in this model, a fundamental mechanism underlying chronic pain, has been debated. Face, construct and predictive validity are key requisites of animal models; electromyogram (EMG) recordings were utilized to objectively demonstrate validity of the rat UVB/HR model. ⋯ This study used objective outcome measures of secondary hyperalgesia to validate the rat UVB/HR model as a translational model of inflammatory pain.