Brain research
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Current research on empathy for pain emphasizes the overlap in the neural response between the first-hand experience of pain and its perception in others. However, recent studies suggest that the perception of the pain of others may reflect the processing of a threat or negative arousal rather than an automatic pro-social response. It can thus be suggested that pain processing of other-related, but not self-related, information could imply danger rather than empathy, due to the possible threat represented in the expressions of others (especially if associated with pain stimuli). ⋯ Those pictures were primed with own or other faces following the same procedure as in Experiment 1 while ERPs were recorded. Early (N1) and late (P3) cortical responses between pain and no-pain were modulated only in the other-face priming condition. These results support the threat value of pain hypothesis and suggest the necessity for the inclusion of own- versus other-related information in future empathy for pain research.
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A prolonged exposure to vibration stimuli triggers pathological changes with many later manifested symptoms. Early vibration-induced changes are still not very well explored. Therefore, short 30 min vibration period per day with frequency 60 Hz repeated for 10 days was used, and the retrograde axonal transport from the sciatic nerve, the expression of calcitonin gene-related peptide (CGRP) and parvalbumin (PV) were studied in the dorsal root ganglia (DRGs) corresponding to lower lumbar spinal levels. ⋯ CGRP protein expression determined by Western blot analysis and optical density measurement, and NGF level measured by ELISA have been decreased, markedly only at the L4 DRG. PV protein expression was not affected by short repeated vibrations. Our results indicate that (a) short-lasting repeated vibrations affect the retrograde axonal transport in the DRG sensory neurons differently than in spinal motor neurons; (b) a decreased NGF-dependent CGRP production in the DRG primary sensory neurons plays an important role in early vibration-induced pathological mechanisms.
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Comparative Study
The respective and interaction effects of spinal GRs and MRs on radicular pain induced by chronic compression of the dorsal root ganglion in the rat.
High levels of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) are colocalized in the substantia gelatinosa. This indicates that the pain pathways appear to be under a strong regulation of these receptors. However, their respective effects on pain behaviors and their interaction remain unclear. ⋯ Moreover, different from intrathecally administered dexamethasone alone [no difference was found between two dose levels of dexamethasone (4 μg=2 μg)], dexamethasone suppresses mechanical allodynia and thermal hyperalgesia in a dose-dependent manner (4 μg>2 μg>vehicle) when combined with spironolactone (3 μg). These findings indicate that both central GRs and MRs play an important role in the regulation of pain behaviors and they have a perplexing interaction with each other. Spironolactone can enhance the analgesic effects of dexamethasone via complex mechanisms.
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The neuroprotective benefit of intra-operative anesthetics is widely described and routinely aimed to invoke electroencephalographic (EEG) silence in anticipation of transient cerebral ischemia. Previous rat survival studies have questioned an additional benefit from achieving EEG silence during transient global cerebral hypoperfusion. Surgical preparation on twelve New Zealand white rabbits under ketamine-propofol anesthesia, included placement of skull screws for bilateral EEG monitoring, skull shaving for laser Doppler probes, and a 5 mm diameter right temporal craniotomy for the NADH probe. ⋯ Compared to controls, the increase in NADH during ischemia was unaffected by EEG silence with either intravenous or intraarterial propofol. We failed to observe any significant additional attenuation of the elevation in NADH levels with propofol induced EEG silence during transient global cerebral hypoperfusion. This is consistent with previous rat survival studies showing that EEG silence was not required for full neuroprotective effects of pentothal anesthesia.
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A growing body of evidence indicates that Toll-like receptors (TLRs) and Interleukin-1 (IL-1) family have been shown to be involved in the damaging inflammatory processes associated with stroke, infection, neoplasia, and other diseases in the central nervous system. Myeloid differentiation primary response protein 88 (Myd88) is a critical adaptor protein that transmits signals for TLRs and IL-1 family. Therefore, this study aimed to detect the expression of Myd88 protein and mRNA in a rat weight-dropping trauma model and to clarify the role of Myd88 after traumatic brain injury (TBI). ⋯ NF-κB, TNF-α, IL-1β and ICAM-1 also ascended significantly after TBI. Our data demonstrated that Myd88 was increasingly expressed in a parallel time course to the up-regulation of NF-κB, proinflammatory cytokines and ICAM-1 and there was a highly positive relationship among them. These findings might have important implications during the administration of specific Myd88 antagonists in order to prevent or reduce inflammatory response after TBI.