Neuroscience
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Randomized Controlled Trial
Effects of Transcranial Static Magnetic Stimulation on Motor Cortex Evaluated by Different TMS Waveforms and Current Directions.
Transcranial static magnetic stimulation (tSMS) modulates cortical excitability probably by interacting with the GABA-glutamate intracortical balance. Different transcranial magnetic stimulation (TMS) waveforms probe distinct GABA-mediated cortical inhibition networks. The goal of the present work is to further characterize tSMS-induced changes in motor cortex reactivity and inhibition-excitation (I/E) balance. ⋯ MEP amplitude increased compared to sham with monoAP TMS, with no clear changes in general intracortical I/E balance. Biphasic TMS was not able to capture any effects of tSMS. The results show that the effects of tSMS on cortical excitability and inhibition involve specific interneuron circuits that are selectively activated by monoPA TMS.
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Randomized Controlled Trial
Fronto-Parietal Brain Areas Contribute to the Online Control of Posture during a Continuous Balance Task.
Neuroimaging studies have provided evidence for the involvement of frontal and parietal cortices in postural control. However, the specific role of these brain areas for postural control remains to be known. Here, we investigated the effects of disruptive transcranial magnetic stimulation (TMS) over supplementary motor areas (SMA) during challenging continuous balance task in healthy young adults. ⋯ Importantly, cTBS over SMA compared to sham stimulation altered EEG power within the identified fronto-parietal regions. These findings suggest that the changes in activation within distant fronto-parietal brain areas following cTBS over SMA contributed to the altered postural behavior. Our study confirms a critical role of AC, CG, and both PPC regions in calibrating online postural responses during a challenging continuous balance task.
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Ketogenic diet is reported to protect against cognitive decline, drug-resistant epilepsy, Alzheimer's Disease, damaging effect of ischemic stroke and many neurological diseases. Despite mounting evidence that this dietary treatment works, the exact mechanism of its protective activity is largely unknown. Ketogenic diet acts systemically, not only changing GABA signaling in neurons, but also influencing the reliance on mitochondrial respiration, known to be disrupted in many neurological diseases. ⋯ In the brain astrocytes are believed to be the sole neural cells capable of fatty oxidation. Here we try to explain that not exclusively neurons, but also morphological changes of astroglia and/or microglia due to different metabolic state are important for the mechanism underlying the protective role of ketogenic diet. By quantifying different parameters describing cellular morphology like ramification index or fractal dimension and using Principal Component Analysis to discover the regularities between them, we demonstrate that in normal adult rat brain, ketogenic diet itself is able to change glial morphology, indicating an important role of these underappreciated cells in the brain metabolism.
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People commonly synchronize taps to rhythmic sounds and can continue tapping after the sounds stop, indicating that time intervals between sounds can be internalized. Here, we investigate what happens in the brain after simply listening to auditory beats in order to understand more about the automatic internalization of temporal intervals without tapping. Electroencephalograms were recorded while musicians attended to accelerating, decelerating, or steady click sequences. ⋯ In contrast, physical beats elicited P2 responses and early beta suppressions, likely reflecting a combination of stimulus-related processing and temporal prediction. These results suggest that the activities observed after the silent beat were not produced via sustained entrainment after the physical beats, but via automatically-formed expectation for an additional beat. Therefore, beta modulations may be generated endogenously by expectation violation, while P3a amplitudes may relate to strength of expectation, with acceleration endings causing the strongest expectations for sequence continuation.
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One deficit associated with schizophrenia (SZ) is the reduced ability to distinguish self-caused sensations from those due to external sources. This reduced sense of agency (SoA, subjective awareness of control over one's actions) is hypothesized to result from a diminished utilization of internal monitoring signals of self-movement (i.e., efference copy) which subsequently impairs forming and utilizing sensory prediction errors (differences between the predicted and actual sensory consequences resulting from movement). Another important function of these internal monitoring signals is the facilitation of higher-order mechanisms related to motor learning and control. ⋯ Although adaptation was similar for SZP and controls, the extent of generalization was significantly less for SZP; movement trajectories made by patients to the furthest untrained target (135o) before and after adaptation were largely indistinguishable. Interestingly, deficits in generalization were correlated with positive symptoms of psychosis in SZP (e.g., hallucinations). Generalization was also associated with measures of SoA across both SZP and HC, emphasizing the role action awareness plays in motor behavior, and suggesting that misattributing agency, even in HC, manifests in abnormal motor performance.