Neuroscience
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Brief noxious heat stimuli activate Aδ- and C-fibers and allow contact heat-evoked potentials (CHEPs) to be recorded from the scalp. Under normal conditions, only late responses related to Aδ-fibers can be recorded. This study aimed to demonstrate C-fiber responses to contact heat stimuli. ⋯ Following nerve compression and capsaicin application, ultralate CHEPs with latencies >800 ms could be recorded in 13 subjects (62%), pain intensity to the contact heat stimuli was increased and the warm/hot-burning pain quality became more intense. The main results of our study are the demonstration of ultralate C-fiber-related CHEPs following A-fiber blockade in 29% of healthy subjects increasing to 62% when the blockade was combined with capsaicin. After blockade of Aδ-fibers we recorded responses with latencies in the range between the latencies of Aδ- and C-fibers suggesting release of Aδ-fibers with slower conduction velocity than normally recorded with CHEPs.
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Proprioceptive signals are of prime importance in kinesthesia. However, in conditions of visuo-proprioceptive conflicts, strong visual-evoked biases can be observed. In three experiments, we parsed the interaction between visual and proprioceptive afferents using the 'mirror box' paradigm. ⋯ For instance, when both sensory channels conveyed signals of arm displacement but in the opposite direction, kinesthetic illusions occurred but were either proprioceptively (vibration illusion) or visually driven (mirror illusion), according to individual sensorial preferences (Experiments 2 and 3). These results indicate that kinesthesia is the product of cooperative integration processes in which the final percept strongly depends on the experimental conditions as well as sensorial preferences. The observed changes in the relative contribution of each input across experimental conditions likely reflect reliability-dependent weights.
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Unilateral damage to the peripheral vestibular receptors precipitates a debilitating syndrome of oculomotor and balance deficits at rest, which extensively normalize during the first week after the lesion due to vestibular compensation. In vivo studies suggest that GABA(B) receptor activation facilitates recovery. However, the presynaptic or postsynaptic sites of action of GABA(B) receptors in vestibular nuclei neurons after lesions have not been determined. ⋯ In uncompensated chickens, baclofen decreased mEPSC frequency to the greatest extent in principal cells on the intact side, with concurrent increases in GABA(B)R2 pixel brightness and percentage overlap in synaptotagmin 1-labeled terminals. Altogether, these results revealed changes in presynaptic GABA(B) receptor function and expression which differed in compensating and uncompensated chickens shortly after UVG. This work supports an important role for GABA(B) autoreceptor-mediated inhibition in vestibular nuclei neurons on the intact side during early stages of vestibular compensation, and a role for GABA(B) heteroreceptor-mediated inhibition of glutamatergic terminals on the intact side in the failure to recover function.
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In the present study, we aimed to identify whether cross-modal priming effect based on short-term experience of ecologically unrelated audio-visual information existed. In the experiment, we employed ecologically unrelated pictures and sounds as visual and auditory stimuli. ⋯ Enhanced induced gamma-band activity (GBA) was also found under the Match condition, and we suggested that induced GBA reflected the association between auditory and visual information to form supra-modal representation, which is top-down modulated by short-term experience of audio-visual information. Event-related potential (ERP) analysis revealed an N400 effect under the Mismatch condition compared to the Match condition, and source reconstruction of N400 effect showed that the biggest difference of activity between two conditions was localized in middle temporal gyrus (MTG), suggesting that MTG played an important role in the mapping process of auditory information onto a temporal semantic network.
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Exercise improves cognitive function, and Brain-Derived Neurotrophic Factor (BDNF) plays a key role in this process. We recently reported that particulate matter (PM) exposure negatively contributed to the exercise-induced increase in human serum BDNF concentration. Furthermore, PM exposure is associated with neuroinflammation and cognitive decline. ⋯ In contrast, gene expression in the condition UFP+exercise did not differ from the control. In the condition UFP+rest, hippocampal expression of NFE2L2 was down-regulated and there was a trend toward down-regulation of BDNF expression compared to the control. This study shows a negative effect of UFP exposure on the exercise-induced up-regulation of BDNF gene expression in the hippocampus of rats.