Neuroscience
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It is known that anxiety (ANX) impairs action-perception coupling. This study tests whether this impairment could be associated with an alteration of the sensorimotor function. To this aim, the cortical activities underlying the sensorimotor function were recorded in twelve volunteers in a reach-to-grasp paradigm, in which the level of ANX and the position of a glass were manipulated. ⋯ Fast-α-EEG desynchronization was reduced under breath-restriction (-37.7%; p<0.05). The results confirm that ANX-related impairment of action-perception coupling co-modulates with theta-sensorimotor rhythm. This finding is discussed as an altered "readiness state" in the reaching-related cortical network, while individuals are anxious.
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Combinations of Ca(2+) channel inhibitors have been proposed as an effective means to prevent excess Ca(2+) flux and death of neurons and glia following neurotrauma in vivo. However, it is not yet known if beneficial outcomes such as improved viability have been due to direct effects on intracellular Ca(2+) concentrations. Here, the effects of combinations of Lomerizine (Lom), 2,3-dioxo-7-(1H-imidazol-1-yl)6-nitro-1,2,3,4-tetrahydro-1-quinoxalinyl]acetic acid monohydrate (YM872), 3,5-dimethyl-1-adamantanamine (memantine (Mem)) and/or adenosine 5'-triphosphate periodate oxidized sodium salt (oxATP) to block voltage-gated Ca(2+) channels, Ca(2+) permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, NMDA receptors and purinergic P2X7 receptors (P2X7R) respectively, on Ca(2+) concentration and viability of rat primary mixed cortical (MC) cultures exposed to hydrogen peroxide (H2O2) insult, were assessed. ⋯ Olig2(+) oligodendroglia and ED-1(+) activated microglia/macrophages were not preserved by any of the inhibitor combinations. These data indicate that following H2O2 insult, limiting intracellular Ca(2+) entry via P2X7R is generally associated with increased cell viability. Protection of NG2+ non-oligodendroglial cells by Ca(2+) channel inhibitor combinations may contribute to observed beneficial outcomes in vivo.
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Gut microbiota colonization is a key event for host physiology that occurs early in life. Disruption of this process leads to altered brain development which ultimately manifests as changes in brain function and behaviour in adulthood. Studies using germ-free (GF) mice highlight the extreme impact on brain health that results from life without commensal microbes. ⋯ In tandem with these clear behavioural alterations we found changes in altered CNS serotonin concentration along with changes in the mRNA levels of corticotrophin releasing hormone receptor 1 and glucocorticoid receptor. Additionally, we found changes in the expression of brain derived neurotrophic factor (BDNF), a hallmark of altered microbiota-gut-brain axis signalling. In summary, this model of antibiotic-induced depletion of the gut microbiota can be used for future studies interested in the impact of the gut microbiota on host health without the confounding developmental influence of early-life microbial alterations.
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Compared to isometric activities, the neural basis of fatigue induced by repetitive tasks has been scarcely studied. Recently, we showed that during short-lasting repetitive tasks at the maximal possible rate (finger tapping for 10 and 30s), tapping rate and maximal voluntary contraction (MVC) force decrease at the end of finger tapping. We also observed larger silent periods (SP) induced by transcranial magnetic stimulation during MVC post finger tapping. ⋯ While indices of excitability increased initially in both tasks, they decreased with the isometric task only when the task was prolonged to 30s. We suggest that the inability to maintain increased levels of spinal excitability during task execution is a neurophysiological mark of fatigue. Our results suggest that the origin of fatigue induced by brief and fast repetitive tasks is not spinal.
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The present study explored the relationship between motor-preparatory electroencephalographic (EEG) activity, motivation, and motor performance (specifically premotor reaction time [RT]). Participants performed a RT task by squeezing a hand dynamometer in response to an auditory "go" signal. We recorded EEG and electromyography to index beta-suppression and premotor RT, respectively. ⋯ Mixed-effect linear regression models showed that monetary incentive predicted premotor RT when controlling for beta-suppression, and beta-suppression independently predicted premotor RT. Thus, it appears motivation and beta-suppression can facilitate motor performance independent of one another. A plausible explanation of this effect is that motivation can affect motor performance independent of the motor cortex by influencing subcortical motor circuitry.