Is transcranial direct current stimulation a potential method for improving response inhibition?

Inhibitory control of movement in motor learning requires the ability to suppress an inappropriate action, a skill needed to stop a planned or ongoing motor response in response to changes in a variety of environments. This study used a stop-signal task to determine whether transcranial direct-current stimulation over the pre-supplementary motor area alters the reaction time in motor inhibition. Forty healthy subjects were recruited for this study and were randomly assigned to either the transcranial direct-current stimulation condition or a sham-transcranial direct-current stimulation condition. All subjects consecutively performed the stop-signal task before, during, and after the delivery of anodal transcranial direct-current stimulation over the pre-supplementary motor area （pre-transcranial direct-current stimulation phase, transcranial direct-current stimulation phase, and post-transcranial direct-current stimulation phase）. Compared to the sham condition, there were significant reductions in the stop-signal processing times during and after transcranial direct-current stimulation, and change times were significantly greater in the transcranial direct-current stimulation condition. There was no significant change in go processing-times during or after transcranial direct-current stimulation in either condition. Anodal transcranial direct-current stimulation was feasibly coupled to an interactive improvement in inhibitory control. This coupling led to a decrease in the stop-signal process time required for the appropriate responses between motor execution and inhibition. However, there was no transcranial direct-current stimulation effect on the no-signal reaction time during the stop-signal task. Transcranial direct-current stimulation can adjust certain behaviors, and it could be a useful clinical intervention for patients who have difficulties with response inhibition.

The right inferior frontal gyrus as pivotal node and effective regulator of the basal ganglia-thalamocortical response inhibition circuit

Background:The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in animal models.However,the pivotal nodes and directed causal regulation within this inhibitory circuit in humans remains con-troversial.Objective:The main aim of the present study was to determine the causal information flow and critical nodes in the basal ganglia-thalamocortical inhibitory circuits and also to examine whether these are modulated by biological factors(i.e.sex)and behavioral performance.Methods:Here,we capitalize on the recent progress in robust and biologically plausible directed causal modeling(DCM-PEB)and a large response inhibition dataset(n=250)acquired with concomitant functional magnetic resonance imaging to determine key nodes,their causal regulation and modulation via biological variables(sex)and inhibitory performance in the inhibitory circuit encompassing the right inferior frontal gyrus(rIFG),caudate nucleus(rCau),globus pallidum(rGP),and thalamus(rThal).Results:The entire neural circuit exhibited high intrinsic connectivity and response inhibition critically increased causal projections from the rIFG to both rCau and rThal.Direct comparison further demonstrated that response inhibition induced an increasing rIFG inflow and increased the causal regulation of this region over the rCau and rThal.In addition,sex and performance influenced the functional architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation,while better inhibitory performance was associated with stronger rThal to rIFG communication.Furthermore,control analyses did not reveal a similar key communication in a left lateralized model.Conclusions:Together,these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.

Attentional orienting and response inhibition: insights from spatial-temporal neuroimaging

Attentional orienting and response inhibition have largely been studied separately. Each has yielded important findings, but controversy remains concerning whether they share any neurocognitive processes. These conflicting findings may originate from two issues： （1） at the cognitive level, attentional orienting and response inhibition are typically studied in isolation; and （2） at the technological level, a single neuroimaging method is typically used to study these processes. This article reviews recent achievements in both spatial and temporal neuroimaging, emphasizing the relationship between attentional orienting and response inhibition. We suggest that coordinated engagement, both top-down and bottom-up, serves as a common neural mechanism underlying these two cognitive processes. In addition, the right ventrolateral prefrontal cortex may play a major role in their harmonious operation.

Potassium channel AKT1 is involved in the auxin-mediated root growth inhibition in Arabidopsis response to low K^+stress

The changes in external K^＋ concentration affect plant root growth. However, the molecular mechanism for perceiving a K^＋ signal to modulate root growth remains unknown. It is hypothesized that the K^＋ channel AKTI is involved in low K^＋ sensing in the Arabidopsis root and subsequent regulation of root growth. Along with the decline of external K^＋ concentration, the primary root growth of wild-type plants was gradually inhibited. However, the primary root of the akt1 mutant could still grow under low K^＋（LK） conditions. Application of NAA inhibited akt1 root growth, but promoted wild-type root growth under LK conditions. By using the ProDR5：GFP and ProPIN1：PIN1-GFP lines, we found that LK treatment reduced auxin accumulation in wild-type root tips by degrading PIN1 proteins, which did not occur in the akt1 mutant. The LK-induced PIN1 degradation may be due to the inhibition of vesicle trafficking of PIN1 proteins. In conclusion, our findings indicate that AKT1 is required for an Arabidopsis response to changes in external K^＋, and subsequent regulation of K^＋-dependent root growth by modulating PINt degradation and auxin redistribution in the root.

Growth inhibition and oxidative damage of Microcystis aeruginosa induced by crude extract of Sagittaria trifolia tubers

Aquatic macrophytes are considered to be promising in controlling harmful cyanobacterial blooms. In this research, an aqueous extract of Sagittaria trifolia tubers was prepared to study its inhibitory effect on Microcystis aeruginosa in the laboratory. Several physiological indices of M. aeruginosa, in response to the environmental stress, were analyzed. Results showed that S. trifolia tuber aqueous extract significantly inhibited the growth of M. aeruginosa in a concentration-dependent way. The highest inhibition rate reached 90% after 6 day treatment. The Chlorophyll-a concentration of M. aeruginosa cells decreased from 343.1 to314.2 μg/L in the treatment group. The activities of superoxide dismutase and peroxidase and the content of reduced glutathione in M. aeruginosa cells initially increased as a response to the oxidative stress posed by S. trifolia tuber aqueous extract, but then decreased as time prolonged. The lipid peroxidation damage of the cyanobacterial cell membranes was reflected by the malondialdehyde level, which was notably higher in the treatment group compared with the controls. It was concluded that the oxidative damage of M. aeruginosa induced by S.trifolia tuber aqueous extract might be one of the mechanisms for the inhibitory effects.

Hydrogen sulfide protects against high glucose-induced H9c2 cardiomyocyte injury and inflammatory response by inhibiting ROS-TLR4 pathway

Objective To investigate whether exogenous hydrogen sulfide（H2S）protects high glucose（HG）-inducedH9c2 cardiomyocyte injury and inflammation response by inhibiting reactive oxygen species（ROS）-Toll-like receptor 4（TLR4）pathway.Methods Cell counter kit-8（CCK-8）assay was used to measure the cell viability,

Characterizing motor impulsivity of individuals classified as overweight to obese

Deficits in the impulse control system are an important predictor of energy intake and body weight.Adults classified as overweight to obese may possess these deficits as a general behavioral trait or they may be foodspecific.The present study assessed motor impulsivity(ability to suppress a pre-potent response)when presented with food and neutral(non-food)cues,testing if deficits in motor impulsivity is specific to food cues or a general trait among participants classified as overweight to obese.The proportion of inhibitory failures to no-go targets following food cues(10.8%)was significantly greater than the proportion of inhibitory failures to no-go targets following neutral cues(1.9%,p<0.001).These differences remained when covering for sex and hunger.This indicates deficits in food-specific impulse control(as opposed to general impulse control)are present in those classified as overweight to obese.Understanding the specific aspect of impulse control that is present in this population is needed for the development of future impulse control training interventions that seek to change eating behaviors as a means for weight control.

Comparison in executive function in Chinese preterm and full-term infants at eight months

Executive function （EF） is increasingly recognized as being responsible for adverse developmental outcomes in preterm-born infants. Several perinatal factors may lead to poor EF development in infancy, and the deficits in EF can be identified in infants as young as eight months. A prospective cohort study was designed to study the EF in Chinese preterm infants and examine the relationship between EF in preterm infants and maternal factors during perinatal period. A total of 88 preterm infants and 88 full-term infants were followed from birth to eight months （corrected age）. Cup Task and Planning Test was applied to assess the EF of infants, and the Bayley Scale of Infant Development （BSID-III） was used to evaluate cognitive （MDI） and motor abilities （PDI） of infants. In comparison with full-term infants, the preterm infants performed more poorly on all measures of EF including working memory, inhibition to prepotent responses, inhibition to distraction, and planning, and the differences remained after controlling the MDI and PDI. Anemia and selenium deficiency in mothers during pregnancy contributed to the differences in EF performance. However, maternal depression, hypertension, and diabetes during pregnancy were not related to the EF deficits in preterm infants. Future research should focus on the prevention of anemia and selenium deficiency during pregnancy and whether supplementing selenium in mothers during pregnancy can prevent further deterioration and the development of adverse outcomes of their offspring.