Brain research
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Motor imagery training is considered as an effective training strategy for motor skill learning and motor function rehabilitation. However, compared with studies of the neural mechanism underlying motor imagery, neuroimaging examinations of motor imagery training are comparatively few. Using functional magnetic resonance imaging, we designed a 2-week motor imagery training experiment, including execution and imagery tasks, to investigate the effectiveness of motor imagery training on the improvement of motor performance, as well as the neural mechanism associated with motor imagery training. ⋯ Our results demonstrated that motor imagery training could improve motor performance. More importantly, the brain functional alterations induced by training were found in the fusiform gyrus for both tasks. These findings provide new insights into motor imagery training.
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Partial sciatic nerve injury is a common model of neuropathic pain in rodents, and produces both mechanical and thermal pain hypersensitivity. Several types of immune cells have been implicated in the pathogenesis of neuropathic pain due to nerve injury; however, the timing of their appearance has not been fully elucidated. Here, using immunohistochemistry, we characterized the time course and magnitude of inflammatory cell infiltration and resident immune cell activation in the sciatic nerves, L3-5 dorsal root ganglia (DRGs) and spinal segments following partial ligation of the sciatic nerve (PSNL) in C57BL/6J mice. ⋯ However, a significant increase in the level of microglial and astrocytic activation was observed in the spinal dorsal horn and to a lesser extent in the ventral horn, peaking on days 7 and 14 after nerve injury. These changes corresponded with a significant increase in immunoreactivity for phosphorylated NR1 subunit of the NMDA receptor, and a significant decrease in IB4-labeled non-peptidergic nociceptive terminals in the ipsilateral dorsal horn. Our findings suggest differential roles for peripheral and central neuroimmune interactions in the production of neuropathic pain.
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Lactate has been identified as an alternative fuel for the brain in situations of increased energy demand, as following a traumatic brain injury (TBI). This study investigates the effect of treatment with sodium lactate (NaLac) on the changes in brain energy state induced by a severe diffuse TBI. Rats were assigned to one of the eight groups (n=10 per group): 1-sham, normal saline; 2-TBI, normal saline; 3-TBI, hypertonic saline; 4-TBI, 100mM NaLac, 5-TBI, 500 mM NaLac; 6-TBI, 1280 mM NaLac; 7-TBI, 2000 mM NaLac and 8-TBI-500 mM NaLac+magnesium sulfate. ⋯ These alterations were not ameliorated with NaLac infusion. We observed a significant reduction in cerebral NAD(+), an essential co-enzyme for mitochondrial lactate-dehydrogenase that converts lactate into pyruvate and thus replenishes the tricarboxylic acid cycle. These results suggest that the metabolic pathway necessary to consume lactate may be compromised following a severe diffuse TBI in rats.