Pain
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The intensity and submodality of pain are widely attributed to stimulus encoding by peripheral and subcortical spinal/trigeminal portions of the somatosensory nervous system. Consistent with this interpretation are studies of surgically anesthetized animals, demonstrating that relationships between nociceptive stimulation and activation of neurons are similar at subcortical levels of somatosensory projection and within the primary somatosensory cortex (in cytoarchitectural areas 3b and 1 of somatosensory cortex, SI). Such findings have led to characterizations of SI as a network that preserves, rather than transforms, the excitatory drive it receives from subcortical levels. ⋯ These studies demonstrate that an extreme anterior position within SI (area 3a) receives input originating predominantly from unmyelinated nociceptors, distinguishing it from posterior SI (areas 3b and 1), long recognized as receiving input predominantly from myelinated afferents, including nociceptors. Of particular importance, interactions between these subregions during maintained nociceptive stimulation are accompanied by an altered SI response to myelinated and unmyelinated nociceptors. A revised view of pain coding within SI cortex is discussed, and potentially significant clinical implications are emphasized.
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microRNAs (miRNAs) are small noncoding RNAs that have been linked to a number of disease-related signal transduction pathways. Several studies indicate that they are also involved in nociception. It is not clear, however, which miRNAs are important and which genes are modulated by miRNA-associated mechanisms. ⋯ Knock-down of miRNA-124a by intravenous administration of a specific miRNA-124a inhibitor further increased the nociceptive behavior associated with an upregulation of the pain-relevant miRNA-124a target MeCP2 and proinflammatory marker genes. In contrast, administration of a miRNA-124a mimic counteracted these effects and decreased nociception by down-regulation of the target gene. In conclusion, our results indicate that miRNA-124a is involved in inflammatory nociception by regulation of relevant target proteins and might therefore constitute a novel target for anti-inflammatory therapy.
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Comparative Study
The effects of prior pain experience on neural correlates of empathy for pain: An fMRI study.
Neuroimaging studies have revealed partially shared neural substrates for both the actual experience of pain and empathy elicited by the pain of others. We examined whether prior pain exposure increased neural activity in the anterior midcingulate cortex (aMCC) and bilateral anterior insula (AI) as a correlate of empathy for pain. Participants (N=64: 32 women, 32 men) viewed pictures displaying exposure to pressure pain (pain pictures) and pictures without any cue of pain (neutral pictures). ⋯ Based on the entire sample, whole brain analyses revealed stronger activation in the retrosplenial cortex, dorsomedial prefrontal cortex, and medial prefrontal cortex in the pain exposure condition. In conclusion, prior pain exposure did not increase, but decreased activity in regions regularly associated with empathy for pain. However, pain experience increased activity in regions associated with memory retrieval, perspective taking, and top-down emotion regulation, which might facilitate empathizing with others.