Neuroscience
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Vision (V) and touch (T) help stabilize our standing body, but little is known on the time-interval necessary for the brain to process the sensory inflow (or its removal) and exploit the new information (or counteract its removal). We have estimated the latency of onset and the time-course of the changes in postural control mode following addition or withdrawal of sensory information and the effect of anticipation thereof. Ten subjects stood in tandem position. ⋯ Changes in postural behavior require a finite amount of time from visual or haptic shift, much longer than reflexes or rapid voluntary responses, suggesting a time-consuming central integration process. This process is longer on addition than removal of haptic information, indicating a heavier computational load. These findings should be taken into account when considering problems of sensorimotor integration in elderly subjects or patients and when designing simulation models of human balance.
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The purpose of this study was to examine whether mechanisms, involved during the maintenance of familiar movement information in memory, were influenced by the degree of familiarity of the display in which the movements were embedded. Twelve gymnasts who possessed high visual and motor familiarity with the movements employed in this study, were recruited. They were invited to retain for a short period of time familiar movements viewed previously and presented under different displays with the aim of recognizing them at a later stage. ⋯ The results in the 13-20 Hz frequency band showed that functional connectivity was greater within the frontal and right temporal areas during the unfamiliar display (i.e., point-light maintenance condition) compared to the familiar display (i.e., video maintenance condition). Differences in functional connectivity between the two maintenance conditions in the beta frequency band are mainly discussed in the light of the process of anticipation. Subjects' perception of the expected difficulty of the upcoming recognition task is discussed.
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We investigated the effects of swimming and treadmill exercise on the level of nerve growth factor (NGF) protein and neurogenesis in the hippocampus, and cognitive function of adult rats over a period of 8 weeks. We divided 144 male Sprague-Dawley rats into 3 groups: (1) a control group (COG; total n=48, n=8 for each time-point), (2) a swimming exercise group (SEG; total n=48; n=8 for each time-point), and (3) a treadmill exercise group (TEG; total n=48, n=8 for each time-point). The SEG and TEG were made to perform their respective exercise type for 5 days per week over a period of 8 weeks. ⋯ Specifically, a significant increase was observed in the SEG at the 3-month time-point. These results show that regular exercise in adult rats increased the level of NGF in the hippocampus, increased the number of newly proliferated nerve cells, and extended the period of neuron survival and maintenance. Furthermore, this phenomenon was more apparent when the exercise form was swimming.
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Previous research has demonstrated that diabetes induced learning and memory deficits. However, the mechanism of memory impairment induced by diabetes is poorly understood. Dietary fatty acids, especially polyunsaturated fatty acids (PUFA), have been shown to enhance learning and memory and prevent memory deficits in various experimental conditions. ⋯ Fish oil dietary supplementation decreased the transient currents and Kv4.2 expression in the hippocampus and partially improved learning performance of diabetic rats. The results of the present study suggested that sodium and potassium currents contributed to the inhibitory effect of diabetes on neuron excitability, further influencing learning and memory processing. Dietary fish oil may modulate the membrane excitability and is a possible strategy for preventing the impairments of diabetes on hippocampal function.
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MMP-9 deficiency protected against photochemical thrombosis-induced brain hemorrhagic transformation (HT), but it did not protect against tissue plasminogen activator-induced brain hemorrhage. The roles of MMP-2 and/or MMP-9 knockout (KO) in mechanical reperfusion induced HT after ischemia have not been investigated. Here we assessed the effects of MMP-2 KO, MMP-9 KO and MMP-2/9 double KO (dKO) in protecting against mechanical reperfusion induced HT and other brain injuries after the early stages of cerebral ischemia in mice of the same genetic background. ⋯ WT). The results suggested that MMP-2 deficiency and MMP-2 and MMP-9 double deficiency were more protective than MMP-9 deficiency against HT after the early stages of ischemia and reperfusion. These studies increase our understanding of MMP-2 and MMP-9 in HT development and will help to selectively target MMPs to protect the post-ischemic brain from injury and HT.