Neuroscience
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Individuated finger movements represent a key feature of hand dexterity. However, our understanding of mechanisms underlying the acquisition of this motor skill is limited. The present study aimed to identify the effects of daily motor training on acquisition of individuated finger movements. ⋯ The decrease was more pronounced in the pair of fingers with lower independent control prior to the practice. Furthermore, a few finger pairs demonstrated facilitated movement independence when the subject was provided with visual feedback (VFB) regarding the rhythmic accuracy of motor actions following each practice. The results provide evidence for the enhancement of individuated finger movements through dexterous hand use during piano practice, which suggests plastic adaptation of the neuromuscular system associated with independent control of finger movement.
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Encoding muscular force output during voluntary contractions is widely perceived to result, at least in part, from modulations in neuronal activity within the sensorimotor cortex. However the underlying electrophysiological phenomena associated with increased force output remains unclear. This study directly assessed sensorimotor cortex activity using electroencephalography (EEG) in humans performing isometric knee-extensions at a range of discrete torque levels. ⋯ Conversely, activity within the other frequency bands was not modulated by torque (P≥0.09), nor was overall CCD (P=0.11). Peripheral neuromuscular activation (quadriceps electromyography (EMG) amplitude) demonstrated distinct increases between each torque level (P<0.01). In conclusion, sensorimotor cortical activity within the gamma band demonstrated an overall increase with contraction torque, whereas both CCD and each of the other constituent frequency bands were not modulated by increments in torque magnitude during isometric knee-extension contractions up to 60%MVT.
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The brains of diving mammals are repeatedly exposed to hypoxic conditions during diving. Brain neurons of the hooded seal (Cystophora cristata) have been shown to be more hypoxia tolerant than those of mice, but the underlying mechanisms are not clear. Here we investigated the roles of different metabolic substrates for maintenance of neuronal activity and integrity, by comparing the in vitro spontaneous neuronal activity of brain slices from layer V of the visual cortex of hooded seals with those in mice (Mus musculus). ⋯ Indeed, we found about three times higher glycogen stores in the seal brain (∼4.1 ng per μg total protein in the seal cerebrum) than in the mouse brain. Notably, in aCSF containing no glucose, seal neurons can tolerate 20 mM lactate while in mouse neuronal activity vanished after few minutes even in normoxia. This can be considered as an adaptation to long dives, during which lactate accumulates in the blood.
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Odor-evoked responses in mitral cells of the olfactory bulb are characterized by prolonged patterns of action potential (spike) activity. If downstream neurons are to respond to each spike in these patterns, the duration of the excitatory response to one spike should be limited, enabling cells to respond to subsequent spikes. To test for such mechanisms, we performed patch-clamp recordings in slices of the mouse anterior piriform cortex. ⋯ This inhibition tracked the timing of the first spike in SP cells across conditions, which naturally limited the spike number to 1-2. These response features to LOT stimulation were, moreover, not unique to SP cells, also occurring in a population of fluorescently labeled interneurons in glutamic acid decarboxylase 65-eGFP mice. That these different cortical cells respond to incoming inputs with 1-2 spikes per stimulus may be especially critical for relaying bulbar information contained in synchronized oscillations at beta (15-30Hz) or gamma (30-80Hz) frequencies.
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The laggard (lag) mutant mouse, characterized by hypomyelination and cerebellar ataxia, is a spontaneously occurring mutant mouse caused by mutation in the Kif14 gene. In this mutant mouse, the laminated structures such as the cerebral and cerebellar cortices and the dentate gyrus are cytoarchitecturally abnormal. Macroscopically, the olfactory bulb of the lag mutant mouse is smaller in size and more transparent than the normal counterpart. ⋯ In the mutant, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells in the subventricular zone of the lateral ventricle are increased in number, especially at perinatal age, suggesting that the decreased population of granule cells in the lag mutant mouse is caused by the increased apoptotic cell death. The olfactory input appears to be intact, as indicated by anterograde labeling of olfactory nerves with an injection of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) into the olfactory mucosa. In conclusion, the olfactory bulb of the lag mutant mouse is cytoarchitecturally affected, suggesting that the causal gene for lag mutation, i.e., Kif14, has multiple effects on the development of laminated structures in the central nervous system in addition to the myelin formation.