Neuroscience
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Randomized Controlled Trial Comparative Study
What does autonomic arousal tell us about locomotor learning?
Walking onto a stationary sled previously experienced as moving induces locomotor aftereffects (LAE, or "broken escalator phenomenon"). This particular form of aftereffect can develop after a single adaptation trial and occurs despite subjects being fully aware that the sled will not move. Here, we investigate whether such strong LAE expression may relate to arousal or fear related to instability during the gait adaptation process. ⋯ Hence, gait velocity and trunk sway components of the LAE are differentially related to kinematic and autonomic parameters during the early and late adaptation phase. The finding that EDA is a predictor of LAE expression indicates that autonomic arousal or fear-based mechanisms can promote locomotor learning. This could in turn explain some unusual characteristics of this LAE, namely its resistance to explicit knowledge and its generation with just a single adaptation trial.
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Comparative Study
Categorical perception of lexical tones in Chinese revealed by mismatch negativity.
The present study investigated the neurophysiological correlates of categorical perception of Chinese lexical tones in Mandarin Chinese. Relative to standard stimuli, both within- and across-category deviants elicited mismatch negativity (MMN) in bilateral frontal-central recording sites. The MMN elicited in the right sites was marginally larger than in the left sites, which reflects the role of the right hemisphere in acoustic processing. ⋯ These results provide strong neurophysiological evidence in support of categorical perception of lexical tones in Chinese. More important, they demonstrate that acoustic and phonological information is processed in parallel within the MMN time window for the perception of lexical tones. Finally, homologous nonspeech stimuli elicited similar MMN patterns, indicating that lexical tone knowledge influences the perception of nonspeech signals.
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Comparative Study
Estrogen receptor α and G-protein coupled receptor 30 mediate the neuroprotective effects of 17β-estradiol in novel murine hippocampal cell models.
The hippocampus is a multifaceted, complex brain structure considered to be the learning center. The use of primary hippocampal cell cultures has uncovered important cellular mechanisms involved in overall physiological function. Yet, the use of primary culture is inherently difficult, and the lack of immortalized cell lines from the murine hippocampus for mechanistic studies at the molecular level is evident. ⋯ Pretreatment with the GPR30 agonist G-1 (10 and 100 nM) for 1 h, but not 24 h, significantly attenuated cell death in both mHippoE-14 and mHippoE-18 cells. The use of specific ER antagonist ICI 182780 and GPR30 antagonist G-15 linked these effects to both ER and GPR30 receptors. This is the first evidence that GPR30 may play a role in the protective effects of estrogen in hippocampal neurons.
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Comparative Study
Sleep-wakefulness in alcohol preferring and non-preferring rats following binge alcohol administration.
The alcohol-preferring (P) rat is a valid animal model of alcoholism. However, the effect of alcohol on sleep in P or alcohol non-preferring (NP) rats is unknown. Since alcohol consumption has tremendous impact on sleep, the present study compared the effects of binge alcohol administration on sleep-wakefulness in P and NP rats. ⋯ This is the first study that: (1) demonstrates spontaneous sleep-wake profile in P and NP rats, and (2) compares the effects of binge ethanol treatment on sleep in P and NP rats. Our results suggest that, as compared to NP rats, the P rats were more susceptible to sleep disruptions after binge ethanol treatment. In addition, the P rats exhibited insomnia-like symptoms observed during abstinence from alcohol in human subjects.
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Comparative Study
Quinolinate induces selective loss of melanin-concentrating hormone neurons, rather than orexin neurons, in the hypothalamus of mice and young rats.
Orexins are neuropeptides produced in the lateral hypothalamus and implicated in regulation of sleep-wake cycle. Selective loss of orexin neurons is found in the brain of patients with narcolepsy, but the mechanisms of this pathological change are unclear. A previous study showed that excessive stimulation of N-methyl-d-aspartate (NMDA) receptors by quinolinic acid (QA) caused selective loss of orexin neurons in rat hypothalamic slice culture. ⋯ A significant decrease in the number of orexin neurons was induced when QA injection was performed in the dark phase of diurnal cycle, but the degree of the decrease was still lower than that in the number of MCH neurons. Finally, QA (60 nmol) induced selective loss of MCH neurons also in young rats at 3-4 weeks of age. These results do not support the hypothesis that acute excitotoxicity mediated by NMDA receptors is responsible for the pathogenesis of narcolepsy.