Neuroscience
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Robust locomotion is critical to many species' survival, yet the mechanisms by which efficient locomotion is learned and maintained are poorly understood. In mice, a common paradigm for assaying locomotor learning is the rotarod task, in which mice learn to maintain balance atop of an accelerating rod. However, the standard metric for learning in this task is improvements in latency to fall, which gives little insight into the rich kinematic adjustments that accompany locomotor learning. ⋯ By the second week of training, mice began to use a more variable locomotor strategy, where consecutive overshoots or undershoots in strides were selected across paws to drive forward and backward exploration of the wheel. Collectively, our results suggest that mouse locomotor learning occurs through multiple mechanisms evolving over separate time courses and involving distinct corrective actions. These data provide insights into the kinematic strategies that accompany locomotor learning and establish an experimental platform for studying locomotor skill learning in mice.
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Anesthesia and surgery are associated with perioperative neurocognitive disorders (PND). Dexmedetomidine is known to improve PND in rats; however, little is known about the mechanisms. Male Sprague-Dawley rats were subjected to resection of the hepatic apex under propofol anesthesia to clinically mimic human abdominal surgery. ⋯ Rats from the M group showed significantly greater expression levels of Iba-1 and GFAP compared with the C group and the D group. Rats in the M group demonstrated increased Surf1 and Cytochrome c expression on days 1 and 3, but not day 7; similar changes were not induced in rats in the D group. Dexmedetomidine appears to reverse surgery-induced behavior, mitigate the higher density of Iba-1 and GFAP, and downregulate the expression of Surf1 and Cytochrome c protein in the hippocampus of rats in a PND model.
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This study was conducted to provide a better understanding of the role of electric field strength in the production of aftereffects in resting state scalp electroencephalography by repetitive transcranial magnetic stimulation (rTMS) in humans. We conducted two separate experiments in which we applied rTMS over the left parietal-occipital region. Prospective electric field simulation guided the choice of the individual stimulation intensities. ⋯ Relative to baseline, alpha power was significantly reduced by the arrhythmic protocol, while there was no significant change with the rhythmic protocol. We found no significant long-term, i.e., up to 10-second, differences between the rhythmic and arrhythmic stimulation, or between the rhythmic and sham protocols. Weak arrhythmic rTMS induced short-lived alpha suppression during the inter-burst intervals.
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Congruent visual information enhances auditory speech perception. This visual benefit has been widely observed in perception of consonants and vowels, and linked to reduced amplitudes and latencies of auditory N1 and P2 event-related potential (ERP) components when visual information was present. However, it remains unclear whether lexical tone perception in Mandarin also shows this visual benefit. ⋯ Result showed amplitude reductions in N1/P2 and a latency reduction in N1 for audiovisual lexical tone perception. These findings suggest that lexical tone perception was also helped by visual information as found in consonants. Furthermore, this visual benefit in N1 for lexical tone perception was delayed relative to consonants.
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The N-methyl-d-aspartate receptor (NMDAR) is a glutamate-gated receptor channel that plays a role in peripheral neuropathic pain. Src, a protein tyrosine kinase, can regulate the activation of NMDARs in chronic pain conditions. Pannexin 1 (Panx1), a plasma membrane channel, plays an important role in neuropathic pain and functionally interacts with NMDARs in the pathological condition of epilepsy. ⋯ Similarly, PP2 (an inhibitor of Src) also decreased Panx1 protein expression but had no effect on NR1. In addition, intraganglionic injection of 10Panx (a blocker of Panx1) decreased NR1 protein expression but did not affect Src. In general, our findings demonstrated that NR1, Src, and Panx1 all contributed to orofacial ectopic pain following IANX and that they composed a signalling pathway in the TG involved in mechanical allodynia.