Neuroscience
-
Accumulating evidence supports that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase contributes to microglia-mediated neurotoxicity in the CNS neurodegenerative diseases. Several studies, including ours, suggest that microglial activation is involved in the retinal degeneration in the animal models of retinitis pigmentosa (RP). In the present study, we investigated the activation of NADPH oxidase in the rod degeneration in rd mice and further explored its role in the microglia-mediated photoreceptor apoptosis. ⋯ Apocynin markedly reduced the production of superoxide radicals and preserved the rod cells. The results suggested that NADPH oxidase might play an important role in the rod degeneration in the rd mice. Inhibition of NAPDH oxidase could be a possible approach to treat RP in the early degenerative stage.
-
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.
-
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.
-
The complement of mechanisms underlying tau pathology in neurodegenerative disorders has yet to be elucidated. Among these mechanisms, abnormal tau phosphorylation has received the most attention because neurofibrillary tangles present in Alzheimer's disease (AD) and related disorders known as tauopathies are composed of hyperphosphorylated forms of this microtubule-associated protein. More recently, we showed that calpain-mediated cleavage leading to the generation of the 17kDa tau₄₅₋₂₃₀ fragment is a conserved mechanism in these diseases. ⋯ Furthermore, functional abnormalities were detected in the transgenic mice using Morris Water Maze and fear conditioning tests. These results suggest that the accumulation of tau₄₅₋₂₃₀ is responsible, at least in part, for neuronal degeneration and some behavioral changes in AD and other tauopathies. Collectively, these data provide the first direct evidence of the toxic effects of a tau fragment biologically produced in the context of these diseases in vertebrate neurons that develop in situ.
-
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.