Experimental Brain Research最新文献

Visual motion signals are useful in predicting the future, and can affect the detectability and phenomenology of vision in various ways. Recent research has demonstrated that the disappearance position of a moving object is perceived as shifted in the direction of motion when the background consists of dynamic noise. This "twinkle-goes" illusion is thought to arise from a positional prediction overshoot that occurs because dynamic noise delays the accumulation of sensory evidence needed to register the disappearance. In Experiment 1, we examined the temporal dynamics of this illusion by measuring the illusory position shift using a probe at various positions along the motion trajectory and at different time points after the object's physical vanishing. The illusory position shift was nearly zero at the moment the moving object vanished, and subsequently gradually increased as a function of time up to ~ 120 ms after vanishing. In Experiment 2, motivated by prior reports of rhythmic fluctuations in both behavior and neural activity, we investigated whether neural theta oscillations were involved in the illusion. We found that the size of the illusory position shift correlated with the theta phase before vanishing. Taken together, these results suggest that the positional prediction of a moving object is slow-paced and rhythmically updated in synchrony with theta oscillations.

Signal Transducer and Activator of Transcription 1 (STAT1) is a nuclear transcription factor involved in multiple biological processes including the cell cycle, cell survival and immune response. However, the role and mechanism of STAT1 overexpression in learning and memory of young mice have not been investigated. Here, we indicated that STAT1 overexpression apparently induced cognitive defects of 2-month-old C57 mice. STAT1 overexpression in 2-month-old C57 mice markedly decreased spine density and the levels of synaptic associated protein including PSD95, SYN I and PSD93. Moreover, neuronal apoptosis was remarkably induced in STAT1-overexpression 2-month-old C57 mice by BCL-2/Bax signaling pathway. Furthermore, STAT1 overexpression in 2-month-old C57 mice apparently increased the proliferation of microglia and astrocytes, accompanied by a notable elevation in the mRNA levels of inflammatory factors including TNF-α, IL-1α, IL-6 and IL-18. In addition, STAT1 overexpression in 2-month-old C57 mice impaired mitochondrial function by increasing lipid peroxidation levels, decreasing ATP levels and superoxide dismutase activity. Proteomic analysis showed that protein expression profile of synapses, inflammation and mitochondria were all altered and that biological process of synaptic transmission, inflammatory response and fatty acid beta-oxidation were regulated via overexpressing STAT1 in 2-month-old C57 mice. Taken together, these findings suggest that STAT1 may be a pivotal risk factor for impaired cognitive ability.

Given the vestibular system's important role in the perception of upright, we investigated the possible effects of galvanic vestibular stimulation (GVS) on the perception of one's own upright body orientation in relation to gravity, the so-called 'Subjective Postural Vertical (SPV)'. Two groups of healthy participants with an average age of 25.4 years and 64.5 years respectively, each consisting of 28 healthy participants, sat (blindfolded) on a tilting chair. The subjects' feeling of being upright was tested under three different conditions of GVS: right-sided anodal stimulation, left-sided anodal stimulation, and sham stimulation. Our findings revealed that right-sided anodal GVS significantly altered the SPV in both age groups, whereas left-sided anodal GVS did not. The observed effect of GVS on perceived upright body posture was numerically small (up to 0.87° on average) and not due to a loss of sensitivity to the perception of body verticality. The unexpected asymmetry of the behavioral effects of GVS could be related to the known right hemispheric asymmetry of cortical activation in vestibular projection areas, which would need to be further clarified in future studies.

Aging leads to various changes in nervous system functions. Older humans and animals exhibit altered movement patterns and experience alterations in memory and motor functions. Rodent models, particularly aged C57BL/6 mice, have been instrumental in studying behavioral and neurophysiological changes associated with aging. This study aimed to characterize age-related cognitive and motor decline and examine its association with molecular changes in a physiologically aged murine model. For this purpose, female C57BL/6Cenp mice aged 2, 20, and 26 months were used. Several behavioral tests were conducted to evaluate motor and cognitive functions. Additionally, gene expression levels were analyzed in prefrontal cortex and hippocampus samples. Twenty-month-old mice exhibited reduced muscle strength, altered gait patterns, impaired balance on the rotarod test, and deficits in spatial reference memory as assessed by the Barnes maze. Motor function further deteriorated in senescent mice (26-month-old), accompanied by spatial memory impairment as assessed using forced Y-maze test. Moreover, significant changes were observed in the expression of genes associated with synaptic plasticity (ARC, CREB1), neuronal activity (FOS), myelination (OLIG1, MAL), and oxidative stress (CYBA, CYBB, NCF1). These findings confirm that aging is a complex phenomenon marked by progressive cognitive and motor impairments, driven by molecular changes in brain regions involved in critical functions such as motor processes and cognition.

The vestibulospinal and reticulospinal tracts play a crucial role in controlling lumbar erector spinae (LES). Electrical vestibular stimulation (EVS) can be used to investigate the contribution of the vestibular system in the control of a muscle during a motor task. A recent study observed a minimal contribution of the corticospinal projection to LES in a voluntary spine extension. We thus hypothesised a greater involvement of alternative pathways originating in the brainstem such as vestibulo- and reticulospinal tracts in the control of LES for this task. This study investigates the impact of EVS on the activation of LES during postural and voluntary tasks. Fifteen participants performed two motor tasks: a bilateral shoulder flexion (postural task) and a lumbar spine extension (voluntary task) during a simple precued reaction time (RT) paradigm. During the RT tasks, EVS was applied at three different timings (early, middle and late) within a pre-defined time window. Outcomes were (1) LES onset latencies elicited by the motor tasks and conditioned by EVS and (2) the central processing duration (CPD). EVS significantly reduced the onset latency of LES activation in both postural and voluntary tasks. The CPD was shorter for the postural compared to the voluntary task for the early and middle conditions. EVS shortens LES onset, suggesting a contribution of brainstem networks/tracts in both tasks. The shorter CPD for the postural task at early and middle timings compared to the voluntary task suggests an earlier contribution of the brainstem networks/tracts during the postural task. Further research is needed to elucidate the mechanisms and validate this paradigm.im.

Children born very preterm (VPT, ≥ 28 to < 32 gestational weeks) and extremely preterm (EPT, < 28 weeks) are at higher risk for autistic traits and biological motion (BM) processing deficits. Thus, we aimed to examine links between autistic traits and a condensed BM interpretation assessment, as well as potential group differences in performance in 12-year-old children born preterm and full-term. Four short BM stimuli (point-light-walkers) in two noise levels were presented to 25 EPT, 53 VPT and 48 full-term 12-year-old children. Accuracy in BM interpretation was compared across groups and analyzed with parental ratings on the Social Responsiveness Scale 2, adjusting for neonatal characteristics and intelligence. Interactions between preterm status and BM interpretation accuracy with autistic traits were explored. Results showed that the children born EPT had poorer accuracy interpreting BM than the other groups, and children born VPT showed poorer accuracy BM interpretation in high noise compared with the full-term group. BM interpretation accuracy was linked to autistic traits in the EPT and VPT groups. Children born preterm with the poorest BM interpretation accuracy also exhibited the most autistic traits. We concluded that the condensed assessment found prematurity-related deficits in BM interpretation. Performance was strongly linked to autistic traits in the preterm groups, highlighting the relevance of BM interpretation for social reciprocity in children born VPT and EPT.

Healthy adults (OA) achieve rapid isometric force production with a brief, high amplitude burst of neural excitation. In some people with Parkinson's disease (PwPD), transient reductions in neural excitation (motor segmentation) reduce rates of force development (RFD) and prolong contractions. Segmentation has strong relationships with time and rate-based measures of slowing in rapid contractions and is reliably measured from the second derivative of force (F"(t)). We sought more information about how segmentation affects neuromuscular control in PwPD. Aim 1 was to determine the prevalence of PwPD with segmentation (PD_Seg). Aim 2 was to determine how force performance differs in PD_Seg, PwPD without segmentation (PD_NoSeg), and OA. Aim 3 was to quantify force segment durations. Fifty-seven PwPD ON medication and 22 OA performed rapid isometric finger abduction contractions to 20-60% of maximal voluntary contraction force. The median number of force segments to 90% of peak force were measured from F"(t) zero crossings. Additional outcomes included median times to peak force (tPF) and peak RFD (tRFD), and peak RFD (RFDpk). 68% of PwPD had segmentation (median segments ≥ 2, 95% CI [0.55 0.80]). PD_Seg had slower tPF, tRFD and RFDpk than PD_NoSeg and OA (all p ≤ 0.012, 0.38 ≤ r ≤ 0.85). PD_NoSeg and OA did not have statistically different tPF, tRFD, or RFDpk (p > 0.05). PD_Seg had consistent segment durations (coefficient of variation ≤ 25.5%) and shorter first segment durations compared to PD_NoSeg and OA (p < 0.001, r ≥ 0.68), indicating PD_Seg had reduced neuromuscular excitation prior to peak force. Segmentation identifies specific pathophysiology in neuromuscular control that exacerbates slowing in isometric force production.

This is a randomized crossover study design. We examined the acute effects of prolonged social media use (SMU) vs. computerized Modified Stroop Task (MST) on electroencephalogram (EEG) spectral power and physical performance in taekwondo (TKD) athletes. Fifteen athletes underwent cognitive manipulations (SMU, MST, documentary [DOC]), followed by mental tiredness checks (Visual Analogue Scale [VAS]), EEG measurements, an intermittent TKD task, and psychobiological variables (heart rate [HR], rating perceived exertion [RPE]). Only MST significantly increased the VAS (p < 0.05). Theta power decreased in the parietal cortex after cognitive manipulations across conditions (p < 0.001). MST presented a time effect for theta, alpha 1, and alpha 2 in parietal cortex during the task at 15 min (ps < 0.004), diminishing over time. Physical performance declined throughout rounds (p < 0.001), more under MST vs. DOC (p = 0.03). RPE increased (p < 0.001); no significant difference in HR was found (ps > 0.07). High cognitive demand tasks may impair the performance of TKD athletes.

Interhemispheric inhibition (IHI) acts between hemispheres to decrease motor cortical excitability. IHI changes during movement preparation, but it is unknown whether altering IHI, independent of other factors, alters movement initiation. For the index finger abductor muscle (first dorsal interosseous; FDI), IHI is weaker during contralateral index abduction than adduction. Thus, this study aimed to modulate IHI through contralateral contraction and measure resultant changes in reaction time. Fifteen healthy participants (age 19-39 years) completed a reaction-time task requiring brief left index finger abduction. Prior to reactions, participants started either a sustained isometric abduction or adduction contraction of the right index finger. Single- or paired-pulse transcranial magnetic stimulation (TMS) elicited motor evoked potentials (MEPs) from left FDI in the late pre-movement phase. For each contralateral contraction direction, unconditioned and conditioned MEPs (preceded by suprathreshold TMS over the other hemisphere at 10 or 40 ms) were recorded. Conditioned MEPs, expressed relative to unconditioned MEPs, provided measures of short-interval IHI (SIHI) and long-interval IHI (LIHI). Left index finger reaction time was also measured. Linear mixed models showed that reaction time was 9 ± 9 ms (6%) slower during right adduction than abduction (F_1,1875 = 30.7, p < 0.001). Unconditioned MEPs in left FDI were 1.1 ± 2.0 mV (37%) smaller (F_1,270 = 8.82, p = 0.003) and SIHI 11 ± 16% stronger during right adduction (F_1,279 = 15.15, p < 0.001). However, LIHI was not different between right contraction conditions (F_1,272 = 0.410, p = 0.522). These results suggest that IHI can alter reaction time by influencing corticospinal excitability. Stronger SIHI during right adduction likely delayed pre-movement increases in corticospinal excitability, slowing reaction time.

Bupivacaine is a commonly used local anesthetic in both human and equine medicine. This study aimed to explore the molecular mechanism of bupivacaine-induced postoperative cognitive dysfunction (POCD). Bioinformatics analysis identified YES proto-oncogene 1 (YES1) as a key player. A POCD mouse model was developed using bupivacaine and surgery, followed by assessment of cognitive function and DNA damage. SH-SY5Y cells were exposed to bupivacaine, and DNA damage was analyzed. Verteporfin, a Yes-associated protein 1 (YAP1) inhibitor, was used in both mice and cells to study its effects. Bupivacaine increased escape latency and decreased the number of platform crossings in the Morris water maze test, and reduced total distance traveled in the open field test and discrimination index in the novel object recognition test, which was associated with the suppression of YES1 expression in the hippocampal tissue of mice. YES1 overexpression alleviated POCD and neuronal DNA damage induced by bupivacaine in mice by promoting YAP1 phosphorylation. Treatment with verteporfin reversed the alleviating effects of YES1 overexpression on neuronal DNA damage and exacerbated POCD in mice. In conclusion, bupivacaine induces POCD by suppressing YES1 expression and YAP1 phosphorylation, leading to DNA damage.