Pain
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The synaptic vesicle protein synapsin II is specifically expressed in synaptic terminals of primary afferent nociceptive neurons and regulates transmitter release in the spinal cord dorsal horn. Here, we assessed its role in nerve injury-evoked molecular and behavioral adaptations in models of peripheral neuropathic pain using mice genetically lacking synapsin II. Deficiency of synapsin II resulted in reduced mechanical and cold allodynia in two models of peripheral neuropathic pain. ⋯ In addition, the expression of the vesicular glutamate transporters, VGLUT1 and VGLUT2, was strongly reduced in synapsin II knockout mice in the spinal cord. Conversely, synapsin II knockout mice showed a stronger and longer-lasting increase of GABA in lamina II of the dorsal horn after nerve injury than wild type mice. These results suggest that synapsin II is involved in the regulation of glutamate and GABA release in the spinal cord after nerve injury, and that a imbalance between glutamatergic and GABAergic synaptic transmission contributes to the manifestation of neuropathic pain.
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The Child Activity Limitations Interview (CALI) is a measure designed to assess functional impairment due to chronic pain in school-age children. In this study, we present a self-report questionnaire version of the CALI (the CALI-21) that extends the original interview measure. The purpose of this study was to provide internal consistency, cross-informant reliability and construct validity of the CALI-21 on a clinical sample of children and adolescents with chronic pain conditions. ⋯ The CALI-21 showed good internal consistency, high cross-informant reliability, and demonstrated construct validity. The CALI-21 provides increased flexibility via the questionnaire format in the assessment of pain-related activity limitations in children. Factor analysis extends information about specific types of activity limitations experienced by children.
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Chronic pain is a public health problem with high impact on various population segments. There are few population studies with the aim of delineating the profile of the chronic pain patient, and generating data for actions to prevent, control and minimize the problem. The aim of this study was to estimate the prevalence of chronic pain in the population of Salvador, Bahia, Brazil and identify independent predictors associated with this morbidity. ⋯ Among the studied factors, in the gross analysis, the following were shown to be associated with chronic pain: conjugal situation, smoking, excessive alcohol consumption, presence of central obesity and age, all with p<0.05. In the multivariate analysis, female sex, smoking, excessive alcohol consumption, and age were sustained as independent predictors. The presence of chronic pain was predominant in women, the elderly, smokers or ex-smokers and excessive alcohol consumers.
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The standard rodent model of itch uses scratching with the hind limb as a behavioral response to pruritic stimuli applied to the nape of the neck. The assumption is that scratching is an indicator of the sensation of itch. But because only one type of site-directed behavior is available, one cannot be certain that scratching is not a response to nociceptive or other qualities of sensations in addition to, or instead of, itch. ⋯ In contrast, when the same chemicals were injected into the cheek of the mouse, there were two site-directed behaviors: histamine again elicited scratching with the hind limb, but capsaicin evoked wiping with the forelimb. We conclude that the "cheek model of itch" in the mouse provides a behavioral differentiation of chemicals that elicit predominantly itch in humans from those that evoke nociceptive sensations. That is, the model provides a behavioral differentiation between itch and pain in the mouse.
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The glial cytokine, interleukin-1beta (IL-1beta), potentiates the excitability of nociceptive trigeminal ganglion (TRG) neurons via membrane depolarization following peripheral inflammation. Perforated patch-clamp technique was used this study to show that the mechanism underlying the excitability of small-diameter TRG neurons following inflammation is due to IL-1beta. Inflammation was induced by injection of complete Freund's adjuvant (CFA) into the whisker pad. ⋯ IL-1beta inhibited I(A) to a significantly greater extent than I(K). These results suggest that the inhibitory effect of I(A) and I(K) currents by IL-1beta in small-diameter TRG neurons potentiates neuronal excitability thereby contributing to trigeminal inflammatory hyperalgesia. These findings provide evidence for the development of voltage-gated K(+) channel openers and IL-1beta antagonists as therapeutic agents for the treatment of trigeminal inflammatory hyperalgesia.