Focused-attention meditation increases cognitive control during motor sequence performance: Evidence from the N2 cortical evoked potential

Previous work found that single-session focused attention meditation (FAM) enhanced motor sequence learning through increased cognitive control as a mechanistic action, although electrophysiological correlates of sequence learning performance following FAM were not investigated. We measured the persistent frontal N2 event-related potential (ERP) that is closely related to cognitive control processes and its ability to predict behavioural measures. Twenty-nine participants were randomised to one of three conditions reflecting the level of FAM experienced prior to a serial reaction time task (SRTT): 21 sessions of FAM (FAM21, N = 12), a single FAM session (FAM1, N = 9) or no preceding FAM control (Control, N = 8). Continuous 64-channel EEG were recorded during SRTT and N2 amplitudes for correct trials were extracted. Component amplitude, regions of interests, and behavioural outcomes were compared using mixed effects regression models between groups. FAM21 exhibited faster reaction time performances in majority of the learning blocks compared to FAM1 and Control. FAM21 also demonstrated a significantly more pronounced N2 over majority of anterior and central regions of interests during SRTT compared to the other groups. When N2 amplitudes were modelled against general learning performance, FAM21 showed the greatest rate of amplitude decline over anterior and central regions. The combined results suggest that FAM training provided greater cognitive control enhancement for improved general performance, and less pronounced effects for sequence-specific learning performance compared to the other groups. Importantly, FAM training facilitates dynamic modulation of cognitive control: lower levels of general learning performance was supported by greater levels of activation, whilst higher levels of general learning exhibited less activation

ZNF804A genotype modulates neural activity during working memory for faces

Copyright © 2013 S. Karger AG, Basel.Peer reviewedPublisher PD

Deviations in neural activity and network integration underpinning the co-occurrence of emotion dysregulation and attention-deficit/hyperactivity disorder: Analyses of fMRI task activations and functional brain network topology

The aim of this thesis was to improve our understanding of the relationship between Attention-deficit/hyperactivity disorder (ADHD) and emotion dysregulation and the underlying neural activity. Three research articles examine specific aspects of the relationship between ADHD and emotion dysregulation, namely the perception of emotional stimuli, the association between functional brain topology and emotion dysregulation in different ADHD presentations, and emotion dysregulation-related neurobiological and phenotypical predictors of the course of ADHD. All three articles are based on functional magnetic resonance imaging (fMRI) data. Individuals with ADHD exhibited aberrant amygdala reactivity and ventromedial prefrontal cortex coupling in the perception and processing of emotional face stimuli. Moreover, functional network topology of the right insula was shown to affect emotion dysregulation in ADHD and emotion dysregulation and integration of emotion-related brain networks were shown to affect intraindividual change in ADHD severity throughout late adolescence. In Summary, the thesis provides evidence that neural activity and functional connectivity between brain structures affecting emotion may be related to the co-occurrence of emotion dysregulation and ADHD. ADHD and the common co-occurring emotional problems should not be attributed to single, isolated systems, e.g., for executive functions and cognitive control. The neurobiological roots appear to be complex and heterogeneous, involving the interplay of different brain networks that are at least partly emotion-related

Bridging the gap between physiology and behavior: evidence from the sSoTS model of human visual attention

We present the case for a role of biologically plausible neural network modelling in bridging the gap between physiology and behavior. We argue that spiking level networks can allow ‘vertical’ translation between physiological properties of neural systems and emergent ‘whole system’ performance – enabling psychological results to be simulated from implemented networks, and also inferences to be made from simulations concerning processing at a neural level. These models also emphasise particular factors (e.g., the dynamics of performance in relation to real-time neuronal processing) that are not highlighted in other approaches and which can be tested empirically. We illustrate our argument from neural-level models that select stimuli by biased competition. We show that a model with biased competition dynamics can simulate data ranging from physiological studies of single cell activity (Study 1) to ‘whole system’ behavior in human visual search (Study 2), while also capturing effects at ‘intermediate level’, including performance break down after neural lesion (Study 3) and data from brain imaging (Study 4). We also show that, at each level of analysis novel predictions can be derived from the biologically plausible parameters adopted, which we proceed to test (Study 5). We argue that, at least for studying the dynamics of visual attention, the approach productively links single cell to psychological data

Predictive coding as a model of the V1 saliency map hypothesis

The predictive coding/biased competition (PC/BC) model is a specific implementation of predictive coding theory that has previously been shown to provide a detailed account of the response properties of orientation tuned cells in primary visual cortex (V1). Here it is shown that the same model can successfully simulate psy-chophysical data relating to the saliency of unique items in search arrays, of contours embedded in random texture, and of borders between textured regions. This model thus provides a possible implementation of the hypothesis that V1 generates a bottom-up saliency map. However, PC/BC is very different from previous mod-els of visual salience, in that it proposes that saliency results from the failure of an internal model of simple elementary image components to accurately predict the visual input. Saliency can therefore be interpreted as a mechanism by which prediction errors attract attention in an attempt to improve the accuracy of the brain’s internal representation of the world

Looming motion primes the visuomotor system.

A wealth of evidence now shows that human and animal observers display greater sensitivity to objects that move toward them than to objects that remain static or move away. Increased sensitivity in humans is often evidenced by reaction times that increase in rank order from looming, to receding, to static targets. However, it is not clear whether the processing advantage enjoyed by looming motion is mediated by the attention system or the motor system. The present study investigated this by first examining whether sensitivity is to looming motion per se or to certain monocular or binocular cues that constitute stereoscopic motion in depth. None of the cues accounted for the looming advantage. A perceptual measure was then used to examine performance with minimal involvement of the motor system. Results showed that looming and receding motion were equivalent in attracting attention, suggesting that the looming advantage is indeed mediated by the motor system. These findings suggest that although motion itself is sufficient for attentional capture, motion direction can prime motor responses. © 2013 American Psychological Association

Functional organisation of behavioural inhibitory control mechanisms in cortico-basal ganglia circuitry: implications for stimulant use disorder.

The neural and psychological mechanisms of inhibitory control processes were investigated, focusing on the cortico-basal ganglia circuits in rats and humans. These included behavioural flexibility, ‘waiting’ and ‘stopping’ impulsivity and involved serial spatial reversal learning task in rodents, and in humans, premature responses in the Monetary Incentive Delay (MID) task and the stop-signal reaction time task. Chapter 2 and Chapter 3 focus on individual differences in behavioural flexibility in rats while Chapter 4, Chapter 5 and Chapter 6 consider how inhibitory control mechanisms are affected by the psychostimulant drug cocaine in both rats and humans. As reported in Chapter 2, systemic modulation of monoaminergic transmission by monoamine oxidase A (MAO-A) inhibitors enhanced reversal learning performance, selectively by decreasing the lose-shift probability, thereby implicating a role for dopamine, serotonin and noradrenaline in facilitating learning from negative feedback. Resting state functional magnetic resonance imaging (fMRI) revealed enhanced functional connectivity of the orbitofrontal and motor cortices as a correlate of flexible reversal learning performance, consistent with elevated levels of monoamines in these region (Chapter 3). Having clarified the mechanisms underlying behavioural flexibility in rats, Chapter 4 reports that escalation of intravenous cocaine self-administration induces behavioural inflexibility in rats even after a relatively short period of cocaine intake. Computational models, including a reinforced and Bayesian learner, revealed a lack of exploitation of the learned response-outcome relationships in cocaine-exposed rats. Chapter 5 focused on impulse control in human volunteers, identifying the striatal and cingulo-opercular networks as substrates of impulsive, premature responding in healthy 4 volunteers, stimulant-dependent individuals and their unaffected siblings. Loss of impulse control was elicited by different incentives for drug-free participants as opposed to drug users. Drug cues elicited striatal activation and increased premature responses in the stimulant-dependent group compared with the control group. In contrast, the ventral striatum was linked to incentive specific activation to reward anticipation. Task-based fMRI demonstrated that interactions between dorsal striatum and cingulo-opercular “cold cognition” networks underlie failures of impulse control in the control, at-risk and stimulant-dependent groups. However, whereas the cingulo-opercular networks were associated with premature responding in all groups, the reward system was activated specifically by the drug incentive cues in the stimulant group, and by monetary incentive cues in the drug-free groups. Chapter 6 presents evidence that corticostriatal functional and effective connectivity in an overlapping network that includes the anterior cingulate and inferior frontal cortices as well as motor cortex, the subthalamic nucleus and dorsal striatum, is critical to stopping impulse control in both control and cocaine individuals. No stopping efficiency impairments were observed in the cocaine-dependent group. Nevertheless, lower structural corticostriatal connectivity measured using diffusion MRI was associated with response execution impairments in cocaine participants performing a stop-signal reaction time task. Further, response execution was rescued by the selective noradrenaline reuptake inhibitor atomoxetine, which also increased corticostriatal effective connectivity. Finally, increased impulsivity and behavioural inflexibility seen in stimulant use disorder in Chapter 5 and Chapter 4, respectively, were not observed in the endophenotype at risk for developing stimulant abuse but were rather a consequence of stimulant abuse. These results further clarify the monoaminergic substrates of behavioural flexibility and specify the neural and computational impairments in inhibitory control induced by stimulant dependence.Pinsent Darwin Studentship from the Dept of Physiology, Development and Neuroscienc