Background Transcranial direct current stimulation (tDCS) is increasingly used in research and clinical settings, and the dorsolateral prefrontal cortex (DLPFC) is often chosen as a target for stimulation. While numerous studies report modulation of cognitive abilities following DLPFC stimulation, the wide array of cognitive functions that can be modulated makes it difficult to predict its precise outcome. Objective The present review aims at identifying and characterizing the various cognitive domains affected by tDCS over DLPFC. Methods Articles using tDCS over DLPFC indexed in PubMed and published between 2000 and January 2014 were included in the present review. Results tDCS over DLPFC affects a wide array of cognitive functions, with sometimes apparent conflicting results. Conclusion Prefrontal tDCS has the potential to modulate numerous cognitive functions simultaneously, but to properly interpret the results, a clear a priori hypothesis is necessary, careful technical consideration are mandatory, further insights into the neurobiological impact of tDCS are needed, and consideration should be given to the possibility that some behavioral effects may be partly explained by parallel modulation of related functions.
In the adult human brain, the presence of a system matching the observation and the execution of actions is well established. This mechanism is thought to rely primarily on the contribution of so-called 'mirror neurons', cells that are active when a specific gesture is executed as well as when it is seen or heard. Despite the wealth of evidence detailing the existence of a mirror neuron system (MNS) in the adult brain, little is known about its normal development. Yet, a better understanding of the MNS in infants would be of considerable theoretical and clinical interest, as dysfunctions within the MNS have been demonstrated in neurodevelopmental disorders such as autism spectrum disorder. Arguments in favor of an innate, or very early, mechanism underlying action understanding mainly come from studies of neonatal imitation, the existence of which has been questioned by some. Here, we review evidence suggesting the presence of an MNS in the human child, as well as work that suggests, although indirectly, the existence of a mechanism matching the perception and the execution of actions in the human newborn.
In the adult human brain, passive observation of actions performed by others activates some of the same cortical areas that are involved in the execution of actions, thereby contributing to action recognition. This mechanism appears to occur through activation of a population of action-coding cells known as mirror neurons (MN). In the adult motor cortex, performing actions and observing human movement reduces the magnitude of the mu (8-13 Hz) rhythm, possibly reflecting MN system activity. Despite the wealth of information available regarding the adult MN system, little is known about its existence in children. Here, we used EEG to probe mu rhythm modulation in 15 children during observation and execution of hand actions. Our data show that mu rhythm attenuation occurs in children under 11 years old during observation of hand movements. Similarly to what has been reported in adults, observation of goal/object-orientated movement produces greater modulation of the mu rhythm than intransitive movement. These data confirm the existence of an observation-execution matching system in the immature human brain and may be of clinical value in the understanding of neurodevelopmental disorders associated with a faulty MN system, such as autism spectrum disorder.
IMPORTANCE Despite evidence of an association between prenatal acetaminophen exposure and attention-deficit/hyperactivity disorder (ADHD) in offspring, the drug is not contraindicated during pregnancy, possibly because prior studies have relied on maternal self-report, failed to quantify acetaminophen dose, and lacked mechanistic insight.OBJECTIVE To examine the association between prenatal acetaminophen exposure measured in meconium (hereinafter referred to as meconium acetaminophen) and ADHD in children aged 6 to 7 years, along with the potential for mediation by functional brain connectivity. DESIGN, SETTING, AND PARTICIPANTSThis prospective birth cohort study from the Centre Hospitalier Université de Sherbrooke in Sherbrooke, Québec, Canada, included 394 eligible children, of whom 345 had meconium samples collected at delivery and information on ADHD diagnosis. Mothers were enrolled from September 25, 2007, to September 10, 2009, at their first prenatal care visit or delivery and were followed up when children were aged 6 to 7 years. When children were aged 9 to 11 years, resting-state brain connectivity was assessed with magnetic resonance imaging. Data for the present study were collected from September
Since the initial demonstration of linear effects of stimulation duration and intensity on the strength of after-effects associated with transcranial direct current stimulation (tDCS), few studies have systematically assessed how varying these parameters modulates corticospinal excitability. Therefore, the objective of this study was to systematically evaluate the effects of anodal tDCS on corticospinal excitability at two stimulation intensities (1 mA, 2 mA) and durations (10 min, 20 min), and determine the value of several variables in predicting response. Two groups of 20 individuals received, in two separate sessions, 1 and 2 mA anodal tDCS (left primary motor cortex (M1)-right supra-orbital montage) for either 10- or 20-min. Transcranial magnetic stimulation was delivered over left M1 and motor evoked potentials (MEPs) of the contralateral hand were recorded prior to tDCS and every 5 min for 20-min post-tDCS. The following predictive variables were evaluated: I-wave recruitment, stimulation intensity, baseline M1 excitability and inter-trial MEP variability. Results show that anodal tDCS failed to significantly modulate corticospinal excitability in all conditions. Furthermore, low response rates were identified across all parameter combinations. No baseline measure was significantly correlated with increases in MEP amplitude. However, a decrease in inter-trial MEP variability was linked to response to anodal tDCS. In conclusion, the present findings are consistent with recent reports showing high levels of inter-subject variability in the neurophysiological response to tDCS, which may partly explain inconsistent group results. Furthermore, the level of variability in the neurophysiological outcome measure, i.e. MEPs, appears to be related to response.
Activity of the primary motor cortex (M1) during action observation is thought to reflect motor resonance. Here, we conducted three studies using transcranial magnetic stimulation (TMS)-induced motor-evoked potentials (MEPs) of the first dorsal interosseus muscle (FDI) during action observation to determine: (i) the time course of M1 corticospinal excitability during the observation of a simple finger movement; (ii) the specificity of M1 modulation in terms of type of movement and muscle; and (iii) the relationship between M1 activity and measures of empathy and autistic traits. In a first study, we administered single-pulse TMS at 30-ms intervals during the observation of simple finger movements. Results showed enhanced corticospinal excitability occurring between 60 and 90 ms after movement onset. In a second experiment, TMS-induced MEPs were recorded from the FDI and abductor digiti minimi muscles while pulses were delivered 90 ms after movement onset during observation of simple finger movement and dot movement. Increased corticospinal excitability was restricted to finger movement and was present in both muscles. Finally, in an exploratory experiment, single-pulse TMS was administered at 30, 90 and 150 ms after movement onset, and participants were asked to complete the Empathy Quotient (EQ) and the Autism Spectrum Quotient (AQ). Correlational analysis revealed a significant link between motor facilitation at 90 ms and the EQ and AQ scores. These results suggest that corticospinal excitability modulation seen at M1 during action observation is the result of a rapid and crude automatic process, which may be related to social functioning.
The primary objective of this study was to validate French-Canadian versions of the Autism Spectrum Quotient (AQ-F) and the Empathy Quotient (EQ-F) in normal and pathological samples. These versions of the scales were administered to 100 undergraduate university students in the hard science or humanities fields and to 23 individuals diagnosed with autism spectrum disorder (ASD). For both scales, obtained data were partially consistent with English versions. The EQ-F and AQ-F scores were negatively correlated, and the ASD group differed significantly from both control groups, scoring lower on the EQ-F and higher on the AQ-F. These preliminary results support the validity of the AQ-F and EQ-F as screening tools in French-speaking populations.
The human μ-opioid receptor and a mutant form, |iS/ T[i3+Cter]A, in which all Ser and Thr residues from the third cytoplasmic loop and C-terminal domain were changed to Ala, were studied after expression in CHO-K1 cells. Although the mutant receptors had similar affinities for agonists and EC r ,n values for inhibition of adenylyl cyclase as compared to wild-type receptors, the E max were almost 2-fold decreased, suggesting a role of the mutated residues in G-protein coupling. After chronic morphine or etorphine, the EC50 values of the agonists were about 5-fold increased at both receptors but the E max values were not altered; upon agonist withdrawal forskolin-stimulated cAMP levels were increased to almost 200% of control levels. Sequestration and rapid down-regulation of the μ-opioid receptor were induced by DAGO and etorphine but not morphine. In contrast, the μ8/Τ[ί3+ΟεΓ]Α receptor was not sequestered and was up-regulated (150-380%) after treatment with agonists. The results indicate that the Ser and Thr residues in the third cytoplasmic loop and C-terminus of the μ-opioid receptor are not involved in the limited desensitization or in the adenylyl cyclase superactivation promoted by agonists but that their integrity and/ or their phosphorylation is required in the intricate and coordinately regulated pathways involved in receptor signaling and trafficking.
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