Pain
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Comparative Study
Effects of stress on pain threshold and tolerance in children with recurrent abdominal pain.
Models of stress-induced hyperalgesia state that exposure to stress can exaggerate subsequent pain experiences. Studies using both animal and human subjects have shown evidence for hyperalgesia as a function of stress [e.g., Jorum E. Analgesia or hyperalgesia following stress correlates with emotional behavior in rats. ⋯ Children who underwent the stress tasks before the pain task exhibited lower levels of pain tolerance than those who received the pain task first (p<.01); no differences were found between the two groups in pain threshold or pain intensity ratings. Further, pain tolerance was not related to individual differences in physiological reactivity (heart rate change) to the stressor. The present research demonstrates the first evidence of the occurrence of stress-induced hyperalgesia in a pediatric pain population.
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Comparative Study
Species and strain differences in rodent sciatic nerve anatomy: implications for studies of neuropathic pain.
Hindlimb pain models developed in rats have been transposed to mice, but assumed sciatic nerve neuroanatomic similarities have not been examined. We compared sciatic nerve structural organization in mouse strains (C57BL/6J, DBA/2J, and B6129PF2/J) and rat strains (Wistar, Brown Norway, and Sprague-Dawley). Dissection and retrograde labeling showed mouse sciatic nerve origins predominantly from the third lumbar (L3) and L4 spinal nerves, unlike the L4 and L5 in rats. ⋯ Thus, mouse L3 and L4 neural segments are anatomically and functionally homologous with rat L4 and L5 segments. Neuronal changes after distal injury or inflammation should be sought in the mouse L3 and L4 ganglia, and the spinal nerve ligation model in mice should involve ligation of the L4 nerve while L3 remains intact. Strain-dependent variability in segmental contributions to the sciatic nerve may account in part for genetic differences in pain behavior after spinal nerve ligation.
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Comparative Study
Enhanced LTP of primary afferent neurotransmission in AMPA receptor GluR2-deficient mice.
Ca(2+)-permeable-AMPA receptors (AMPARs) are expressed in the superficial dorsal horn (SDH, laminae I/II) of the spinal cord, the area involved in transmission and modulation of sensory information, including nociception. A possible role of Ca(2+)-permeable-AMPARs in synaptic strengthening has been suggested in postnatal DH cultures, but their role in the long-lasting activity-dependent synaptic plasticity of primary afferent neurotransmission in the adult mouse SDH has not been investigated. In the present study the role of Ca(2+)-permeable-AMPARs in the regulation of long-lasting synaptic plasticity, specifically long-term potentiation (LTP) and long-term depression (LTD) in the SDH, was investigated using mice deficient in AMPAR GluR2 subunit. ⋯ The LTP could be induced in the presence of the NMDA receptor antagonist d-AP5, and L-type Ca(2+) channel blockers, suggesting that Ca(2+)-permeable-AMPARs are sufficient to induce LTP in the SDH neurons of adult mouse spinal cord. In contrast, the induction of HFS-LTD is reduced in the SDH of GluR2 mutants. These results suggest an important role for AMPAR GluR2 subunit in regulating synaptic plasticity with potential relevance for long-lasting hypersensitivity in pathological states.
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Comparative Study
Empathy hurts: compassion for another increases both sensory and affective components of pain perception.
Recent studies demonstrate that some brain structures activated by pain are also engaged when an individual observes someone else in pain, and that these empathy-related responses are modulated as a function of the affective link between the empath and the individual in pain. In this study we test the hypothesis that empathy-evoked activation in the pain network leads to heightened pain perception. ⋯ Positive correlations between state empathy scores and pain ratings further suggest that this perceptual phenomenon depends on the magnitude of empathic response induced in the participants. The effects were observed when subjects watched the model receiving either neutral or painful stimuli, suggesting that it is empathy itself that alters pain perception, and not necessarily the observation of pain behaviors.
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Descending modulation of pain can be demonstrated psychophysically by dual pain stimulation. This study evaluates in 31 healthy subjects the association between parameters of the conditioning stimulus, gender and personality, and the endogenous analgesia (EA) extent assessed by diffuse noxious inhibitory control (DNIC) paradigm. Contact heat pain was applied as the test stimulus to the non-dominant forearm, with stimulation temperature at a psychophysical intensity score of 60 on a 0-100 numerical pain scale. ⋯ Importantly, pain scores of the conditioning stimuli were not correlated with EA extent. The latter is based on both our study population, and on additional 82 patients, who participated in another study, in which EA was induced by immersion at 46.5 degrees C. DNIC testing, thus, seems to be relatively independent of the stimulation conditions, making it an easy to apply tool, suitable for wide range applications in pain psychophysics.