Neuroscience
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The aim of this study was to investigate the effects of mental fatigue on the duration of actual and imagined goal-directed arm movements involving speed-accuracy trade-off. Ten participants performed actual and imagined point-to-point arm movements as accurately and as fast as possible, before and after a 90-min sustained cognitive task inducing mental fatigue, and before and after viewing a neutral control task (documentary movie) that did not induce mental fatigue. Target width and center-to-center target distance were varied, resulting in five different indexes of difficulty. ⋯ The trial-by-trial evolution of actual and imagined movement duration remained stable with mental fatigue. The control task did not induce any change in actual and imagined movement duration. The results suggested that movement was slowed in the presence of mental fatigue, maybe due to proactive changes occurring during the preparatory state of the movement, to preserve task success.
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Amplitudes of mu and beta (7-26Hz) oscillations measured by electroencephalography over the sensorimotor areas are suppressed during motor imagery as well as during voluntary movements. This phenomenon is referred to as event-related desynchronization (ERD) and is known to reflect motor cortical excitability. The increased motor cortical excitability associated with ERD during hand motor imagery would induce a descending cortical volley to spinal motoneurons, resulting in facilitation of spinal motoneuronal excitability. ⋯ The right median nerve was stimulated at wrist level when the ERD magnitude of the contralateral hand sensorimotor area exceeded predetermined thresholds during motor imagery. The results showed ERD magnitude during hand motor imagery was associated with an increase in F-wave persistence, but not with the response average of F-wave amplitude or F-wave latency. These findings suggest that the ERD magnitude may be a biomarker representing increases in the excitability of both cortical and spinal levels.
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Mounting experimental evidence, predominantly from male rodents, demonstrates that high-fat diet (HFD) consumption and ensuing obesity are detrimental to the brain. To shed additional light on the neurological consequences of HFD consumption in female rodents and to determine the relatively early impact of HFD in the likely continuum of neurological dysfunction in the context of chronic HFD intake, this study investigated effects of HFD feeding for up to 12weeks on selected behavioral, neurochemical, and electrophysiological parameters in adult female C57BL/6 mice; particular focus was placed on the ventral hippocampus (vHIP). Selected locomotor, emotional and cognitive functions were evaluated using behavioral tests after 5weeks on HFD or control (low-fat diet) diets. ⋯ Mice on HFD also had decreased norepinephrine and dopamine turnover, respectively, in the prefrontal cortex and the vHIP. HFD consumption for a total of 11-12weeks altered vHIP synaptic plasticity, evidenced by significant reductions in the paired-pulse ratio and long-term potentiation (LTP) magnitude. In summary, in female mice, HFD intake for several weeks induced multiple behavioral alterations of mainly anxiety-like nature and impaired monoamine pathways in a brain region-specific manner, suggesting that in the female, certain behavioral domains (anxiety) and associated brain regions, i.e., the vHIP, are preferentially targeted by HFD.
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Prialt, a synthetic version of Ca(v)2.2 antagonist ω-conotoxin MVIIA derived from Conus magus, is the first clinically approved voltage-gated calcium channel blocker for refractory chronic pain. However, due to the narrow therapeutic window and considerable side effects associated with systemic dosing, Prialt is only administered intrathecally. N-triazole oxindole (TROX-1) is a novel use-dependent and activation state-selective small-molecule inhibitor of Ca(v)2.1, 2.2 and 2.3 calcium channels designed to overcome the limitations of Prialt. ⋯ The wind-up response of spinal neurons following repeated electrical stimulation of the receptive field was also unaffected. Spinally applied TROX-1 dose dependently inhibited mechanically evoked neuronal responses in SNL but not sham-operated rats, consistent with behavioral observations. This study confirms the pathological state-dependent actions of TROX-1 through a likely spinal mechanism and reveals a modality selective change in calcium channel function following nerve injury.
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High mortality and morbidity rates are observed in patients with bacterial meningitis (BM) and urge for new adjuvant treatments in addition to standard antibiotic therapies. In BM the hippocampal dentate gyrus is injured by apoptosis while in cortical areas ischemic necrosis occurs. Experimental therapies aimed at reducing the inflammatory response and brain damage have successfully been evaluated in animal models of BM. Fluoxetine (FLX) is an anti-depressant of the selective serotonin reuptake inhibitors (SSRI) and was previously shown to be neuroprotective in vitro and in vivo. We therefore assessed the neuroprotective effect of FLX in experimental pneumococcal meningitis. ⋯ A significant neuroprotective effect of FLX on the hippocampus was observed in acute pneumococcal meningitis in infant rats.