Neuroscience
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In this study, we address the question: Can the central nervous system stabilize vertical posture in the abundant space of neural commands? We assume that the control of vertical posture is associated with setting spatial referent coordinates (RC) for the involved muscle groups, which translates into two basic commands, reciprocal and co-activation. We explored whether the two commands co-varied across trials to stabilize the initial postural state. Young, healthy participants stood quietly against an external horizontal load and were exposed to smooth unloading episodes. ⋯ Analysis of deviations in the {RC; k} space keeping the posture unchanged (motor equivalent) between two states separated by a voluntary quick body sway showed significantly larger motor equivalent deviations compared to non-motor equivalent ones. This is the first study demonstrating posture-stabilizing synergies in the space of neural control variables using various computational methods. It promises direct applications to studies of postural disorders and rehabilitation.
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Overactivated microglia in the spinal cord leads to neuropathic pain sensitivity. The FGF 10, a Fibroblast Growth Factor (FGFs) that is prevalent in neurons, has been demonstrated to suppress microglial polarization. The objective of this study was to investigate the role of FGF 10 in neuropathic pain and the underlying regulatory mechanisms. ⋯ Conversely, GW9662 reversed all beneficial effects of FGF 10 on SNI rats. In addition, phosphorylated levels of NFκB were reduced by pioglitazone or FGF 10 treatment but raised by GW9662 administration in FGF 10-treated SNI rats. Our findings show that FGF 10 has analgesic effects in rats after peripheral nerve injury and justify the role of PPAR-γ/NFκB signaling in FGF 10-regulated anti-microgliosis.
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Wistar Audiogenic Rats (WAR) is an inbred rodent strain susceptible to acute auditory stimulation-induced seizures. However, spontaneous epileptic seizures (SES) and their associated electroencephalogram (EEG) abnormalities have not been reported in WAR kindled animals. The same is true for naïve WARs (without sound-induced seizures). ⋯ The EEG quantitative analysis showed decreased power of cortical delta, theta and beta oscillations in WAR-S, decreased power of cortical fast gamma (FG) oscillations in WARs, independent of microgyria, and decreased interhemispheric synchrony for delta and FG with stronger coupling in delta and theta-FG oscillations in FL animals. The WARs, regardless of microgyria, had reduced locomotor activity, but only WAR-FL animals had reduced anxiety-like behavior. Microgyria in naïve WARs intensified SWD events associated with behavior arrest that could reflect absence-like seizures and abnormal cortical oscillations, and reduced anxiety-like behavior indicating that WAR-FL could be a reliable model to study epileptogenesis.
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Accumulating evidence indicates that repetitive transcranial magnetic stimulation (rTMS) ameliorates motor symptoms in patients with Parkinson's disease (PD); however, patients' responses to rTMS are different. Here, we aimed to explore neural activity changes in patients with PD exhibiting different responses to high-frequency rTMS treatments using functional magnetic resonance imaging (fMRI). We treated 24 patients with PD using 10-session rTMS (10 Hz) over the supplementary motor area (SMA) for 10 days. ⋯ We identified increased fALFF values in the left Crus II of the cerebellar hemisphere and bilateral thalamus as responsive signs to rTMS. Furthermore, the motor response to rTMS over the SMA, measured by the reduction in UPDRS-III and bradykinesia scores, was positively associated with increased fALFF values in the left Crus2 of cerebellar hemisphere, left lobule VIIB of cerebellar hemisphere, right lobule VI of the cerebellar hemisphere, and the right postcentral gyrus. These findings provide evidence for the involvement of cerebellar activity in the motor response to rTMS treatment.
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Aging is a progressive loss of physiological function that increases risk of disease and death. Among the many factors that contribute to human aging, mitochondrial dysfunction has emerged as one of the most prominent features of the aging process. It has been linked to the development of various age-related pathologies, including Parkinson's disease (PD). ⋯ Even though research has shed light on several aspects of the disease pathology, the underlying mechanism of age-related factors responsible for individuals developing this disease is still unknown. This review article aims to discuss the role of mitochondria in the transition from normal brain aging to pathological brain aging, which leads to the progression of PD. We have discussed the emerging evidence on how age-related disruption of mitochondrial quality control mechanisms contributes to the development of PD-related pathophysiology.