Neuroscience
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Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) inhibitors administered prior to or immediately after experimental stroke confer acute neuroprotection. However, it remains unclear if delayed treatment with a PTEN inhibitor improves long-term functional recovery after stroke. We addressed the issue in this study. ⋯ Akt and mTOR activation are the well-established cascades downstream to PTEN inhibition and have been shown to contribute to post-injury axonal regrowth in response to PTEN inhibition. Consistently, in an in vitro neuronal ischemia model, BPV enhanced axonal outgrowth of primary cortical neurons after oxygen-glucose deprivation and the enhancing effects were abolished by Akt/mTOR inhibition. In conclusion, delayed BPV treatment improved functional recovery from experimental stroke possibly via enhancing axonal growth and Akt/mTOR activation contributed to BPV-enhanced post-stroke axon growth.
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We tested a hypothesis that the classical relation between movement time and index of difficulty (ID) in quick pointing action (Fitts' Law) reflects processes at the level of motor planning. Healthy subjects stood on a force platform and performed quick and accurate hand movements into targets of different size located at two distances. The movements were associated with early postural adjustments that are assumed to reflect motor planning processes. ⋯ The magnitude of postural adjustments prior to movement initiation scaled with ID for both short and long distances. Our results provide strong support for the hypothesis that Fitts' Law emerges at the level of motor planning, not at the level of corrections of ongoing movements. They show that, during natural movements, changes in movement distance may lead to changes in the relation between movement time and ID, for example when the contribution of different body segments to the movement varies and when the action of Coriolis force may require an additional correction of the movement trajectory.
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Biofeedback training is an efficient means to gain control over a physiological function typically considered involuntary. Accordingly, learning to self-regulate nociceptive physiological activity may improve pain control by activating endogenous modulatory processes. The aim of the present study was to assess whether trial-by-trial visual feedback of nociceptive flexion reflex (RIII-reflex) responses (an index of spinal nociception) evoked by brief painful shocks applied to the sural nerve could be beneficial to guide participants in adopting strategies aiming at modulating pain perception. ⋯ The biofeedback group was not significantly superior to the sham and the control groups in the modulation of RIII-reflex amplitude, pain intensity or unpleasantness. These results are consistent with the notion that RIII-reflex amplitude and pain perception can be modulated voluntarily by various cognitive strategies. However, immediate retrospective visual feedback of acute nociceptive responses presented iteratively in successive trials may not improve the efficacy of these self-regulation processes.
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This study was designed to examine the effects of chronic running exercise (Ex) on the hypobaric hypoxia-induced neuronal injury in the hippocampus. Male Wistar rats (9 weeks old) were caged in a hypoxic altitude chamber simulating the condition of 9,000 m high (0.303 atm) for 7h and the brains were examined at 0, 4, and 24h after treatment. Hypoxia challenge increased the levels of caspase 3 (mean ± SEM, % of baseline control, 121.9 ± 11.8, 152.3 ± 15.3, 141.6 ± 7.0 for 0, 4 and 24h, respectively, n=5) and induced apoptosis (cell number, 205.7 ± 8.8, 342.3 ± 33.4, 403.0 ± 12.2 for 0, 4 and 24h vs. 7.7 ± 1.4 baseline control, n=3) in the hippocampal CA1 pyramidal neurons. ⋯ Taken together, our results show that chronic Ex protects hippocampal CA1 neurons against hypobaric hypoxia insult. Ex-enhanced bioenergetic adaptation and anti-oxidative capacity may prevent neurons from hypoxia-induced apoptosis. Furthermore, activation of the BDNF signaling pathway may be involved in the Ex-induced protection.
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The relationship between learning/memory performance and long-term potentiation (LTP) induction is ambiguous. Although a large body of data supports a strong correspondence between learning/memory performance and LTP, many studies have also provided evidence to the contrary. In this study, we found that 2-month-old senescence-accelerated mice/prone 8 (SAMP8 mice) displayed both impaired performance in a Morris Water Maze (MWM) and enhanced LTP compared to senescence-accelerated mice/resistance 1 (SAMR1). ⋯ Further analysis demonstrated that the increase in cytokine content was higher in the hippocampal tissues used for LTP recording in the SAMR1 and CFA-challenged animals compared to the SAMP8 and intact BALB/c mice. A correlation analysis demonstrated that pro-inflammatory cytokines (IL-6 and TNF-α) displayed a negative correlation with LTP, while an anti-inflammatory cytokine (IL-10) displayed a positive correlation with LTP. These results suggest that pro-inflammatory cytokines induced by LTP manipulation in experiments (e.g., via tissue injury caused by electrode insertion) may be one of the factors contributing to the observed lack of correspondence between memory/learning ability and LTP.