Brain research
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Neurogenic inflammation (NI) is a feature of several inflammatory pain conditions in which females are overrepresented. Therefore, we asked if there are sex differences in the inflammatory response evoked by well known neurogenic stimuli. We compared the amount of plasma extravasation (PE), a measure of inflammation, in the hindpaw skin of male and female rats caused by subcutaneous injection of capsaicin, application of noxious heat (51 degrees C water bath) or electrical stimulation of the saphenous nerve. ⋯ PE induced by heat was also significantly greater in females compared to males (p<0.001), however, there was no sex-related difference in PE induced by electrical stimulation or by injection of SP. These findings show that females have a greater inflammatory response when inflammation is induced by capsaicin and noxious heat suggesting possible sex-related changes in TRPV-1 receptor mediated mechanisms. These results add to the growing list of sex difference responses to noxious somatic stimulation.
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The spatiotemporal analysis of brain activation during syllogistic reasoning, and the execution of 1 baseline task (BST) were performed in 14 healthy adult participants using high-density event-related brain potentials (ERPs). The following results were obtained: First, the valid syllogistic reasoning task (VSR) elicited a greater positive ERP deflection than the invalid syllogistic reasoning task (ISR) and BST between 300 and 400 ms after the onset of the minor premise. Dipole source analysis of the difference waves (VSR-BST and VSR-ISR) indicated that the positive components were localized in the vicinity of the occipito-temporal cortex, possibly related to visual premise processing. ⋯ Third, both VSR and ISR elicited a more positive ERP deflection than BST between 2500 and 3000 ms. Voltage maps of the difference waves (VSR-BST and VSR-ISR) demonstrated strong activity in the right frontal scalp regions. Results indicate that the reasoning tasks may require more mental effort to spatial processing of working memory.
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Several recent studies suggest that sumo-2/3 modification of proteins occurs following harmful ischemia, however, sumo-2/3-ylation may also be associated with hibernation-mediated neuroprotection. Here we investigate the sumoylation of proteins following ischemia and ischemic tolerance using our established in vitro model of ischemia (oxygen and glucose deprivation; OGD). Following harmful ischemia (120 min OGD), we observed a significant increase in the sumo-2/3-ylation of high molecular weight proteins (>85 kDa), but not sumo-1-ylation of proteins. ⋯ In addition, we observed a reduction in sumo-2/3-ylation using hypothermia (4 degrees C 30 min) as the preconditioning stimuli to induce delayed ischemic tolerance. Further studies show that sumo-2/3-ylation occurs during the ischemic insult and that preconditioning does not change expression of the sumo E1- and E2-ligases (UBA2 and Ubc9) or the sumo specific isopeptidases (SenP1-3). While sumo-2/3-ylation is enhanced under conditions of cell stress, it is not yet clear whether this is a cause or consequence of harmful ischemia-induced cell damage.
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Neural correlates of conscious awareness can be comfortably studied when awareness of the target stimuli is a varying dependent variable in the experimental conditions where the key independent variables are kept invariant. We presented vernier targets backward masked by an invariant grating with invariant SOA. ⋯ Comparison of data from correct aware trials with data from correct unaware trials showed that conscious awareness of targets was associated with decrease in the latency of ERP/P1, increase in the amplitude of P300, and increase in the power of 70-Hz and 30-Hz gamma band oscillations from 50 ms before target onset up to 100 ms after target onset. Results are interpreted in the context of the well-known views about the role of brain-activity oscillations in conscious awareness and as related to the perceptual retouch theory.
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The mas-related genes (Mrgs, also known as sensory neuron-specific receptors, SNSRs) are specifically expressed in small diameter sensory neurons in the trigeminal and dorsal root ganglia, suggesting an important role of the receptors in pain transmission. The present study aimed to investigate the underlying mechanism of the nociceptive effects after activation of MrgC, and the interaction between MrgC and N/OFQ-NOP receptor system in modulation of nociception in mice. Intrathecal (i.t.) administration of [Tyr(6)] gamma2-MSH(6-12), the most potent agonist for MrgC receptor, produced a significant hyperalgesic response as assayed by tail withdrawal test and a series of characteristic nociceptive responses, including biting, licking and scratching, in a dose-dependent manner (0.01-10 pmol and 0.01-10 nmol, respectively) in mice. ⋯ N/OFQ inhibited nociceptive responses at high doses (0.01-1 nmol), but potentiated the behaviors at low doses (1 fmol-3 pmol). Furthermore, both hyperalgesia and nociceptive responses were enhanced after the co-administration with NOP receptor antagonist [Nphe(1)]N/OFQ(1-13)-NH(2). These results suggest that intrathecal [Tyr(6)] gamma2-MSH(6-12)-induced pronociceptive effects may be mediated through NMDA receptor-NO system in the spinal cord, and demonstrate the interaction between MrgC and N/OFQ-NOP receptor system in pain transmission.