Neuroscience
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Effective information transmission for open skill performance requires fine-scale coordination of distributed networks of brain regions linked by white matter tracts. However, how patterns of connectivity in these anatomical pathways may improve global efficiency remains unclear. In this study, we hypothesized that the feeder edges in visual and motor systems have the potential to become "expressways" that increase the efficiency of information communication across brain networks of open skill experts. ⋯ We collected structural imaging data from these subjects, and then resolved structural neural networks using deterministic tractography to identify streamlines connecting cortical and subcortical brain regions of each participant. We observed that superior skill performance in elite athletes was associated with increased information transmission efficiency in feeder edges distributed between orbitofrontal and basal ganglia modules, as well as among temporal, occipital, and limbic system modules. These findings suggest that there is an expressway linking visual and action-control system of skill experts that enables more efficient interactions of peripheral and central information in support of effective performance of an open skill.
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Under pathological conditions, acupoint sensitization is the phenomenon of acupoints transforming from the stable state to the dynamic state. Evidences suggest that hyperpolarization-activated current (Ih), conducted by the hyperpolarization-activated/cyclic nucleotide-gated (HCN) channel, greatly contributes to the peripheral and central sensitization. However, the role of the Ih current in acupoint sensitization has not been explained. ⋯ HCN channel subtype 2 (HCN2) expression levels significantly increased after acupoint sensitization. Furthermore, ZD7288, an HCN current (Ih) blocker, attenuated the acupoint sensitization of the ST35 acupoint. Taken together, our findings suggest that the increased excitability of C- but not Aδ-type neurons and the upregulation of Ih/HCN2 channels contribute to the formation of acupoint sensitization.
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Postural threat decreases center of pressure displacements yet increases the magnitude of movement-related conscious sway perception during quiet standing. It is unknown how these changes influence perception of whole body movement during dynamic stance. The aim of this study was to examine how postural threat influences whole-body movements and conscious perception of these movements during continuous pseudo-random support surface perturbations to stance. ⋯ Trunk sway amplitude remained constant, while tracked movement amplitude increased at height. The gain for perceived to trunk movement was significantly increased at height across frequencies. Threat-related increases in sensitivity of sensory systems related to postural control and changes in cognitive and attention processes may lead to misperceptions of actual movement amplitudes, which may be important when examining increased fall risk in those with a fear of falling.
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Fragile X mental retardation protein (FMRP), a key determinant of normal brain development and neuronal plasticity, plays critical roles in nucleocytoplasmic shuttling of mRNAs. However, the factors involved in FMRP nuclear localization remain to be determined. Using cross-species sequence comparison, we show that an aspartate in position 132 (D132), located within the conserved nuclear localization signal (NLS) of FMRP, appears in human and other mammals, while glutamate 132 (E132) appears in rodents and birds. ⋯ PABP1 knockdown reduces the nuclear localization of human FMRP, but not mouse FMRP. Furthermore, RNase A treatment decreases the PABP1 levels in the anti-V5-immunoprecipitates using the V5-hFMRP-transfected cells, suggesting an interaction between human FMRP and PABP1 in an RNA-dependent fashion. Thus, our data suggest that the FMRP protein with the human-used D132 accommodates a novel protein-RNA-protein interaction which may implicate a connection between FMRP residue transition and neural evolution.
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Hippocampal cholinergic activity enhances long-term potentiation (LTP) of synaptic transmission in intrahippocampal circuits and regulates cognitive function. We recently demonstrated intracellular distribution of functional M1-muscarinic acetylcholine receptors (mAChRs) and neuronal uptake of acetylcholine (ACh) in the central nervous system. Here we examined whether endogenous ACh acts on intracellular M1-mAChRs following its uptake and causes cholinergic facilitation of hippocampal LTP. ⋯ Carbachol (CCh; an AChE-resistant muscarinic agonist) competed with ACh for its uptake and produced cholinergic facilitation of LTP in DFP-untreated slices. The late stage of CCh-induced facilitation was also selectively inhibited by TEA. Our results suggest that when AChE is inactivated by inhibitors, LTP in hippocampal slices is significantly enhanced by endogenous ACh and that cholinergic facilitation is caused by direct activation of cell-surface M1-mAChRs and subsequent activation of intracellular M1-mAChRs after ACh uptake.