Josep Marco-Pallarés

Human oscillatory activity associated to reward processing in a gambling task

Previous event-related brain potential (ERP) studies have identified a medial frontal negativity (MFN) in response to negative feedback or monetary losses. In contrast, no EEG correlates have been identified related to the processing of monetary gains or positive feedback. This result is puzzling considering the large number of brain regions involved in the processing of rewards. In the present study we used a gambling task to investigate this issue with trial-by-trial wavelet-based time-frequency analysis of the electroencephalographic signal recorded non-invasively in healthy humans. Using this analysis a mediofrontal oscillatory component in the beta range was identified which was associated to monetary gains. In addition, standard time-domain ERP analysis showed an MFN for losses that was associated with an increase in theta power in the time-frequency analysis. We propose that the reward-related beta oscillatory activity signifies the functional coupling of distributed brain regions involved in reward processing.

Neural mechanisms underlying adaptive actions after slips

An increase in cognitive control has been systematically observed in responses produced immediately after the commission of an error. Such responses show a delay in reaction time (post-error slowing) and an increase in accuracy. To characterize the neurophysiological mechanism involved in the adaptation of cognitive control, we examined oscillatory electrical brain activity by electroencephalogram and its corresponding neural network by event-related functional magnetic resonance imaging in three experiments. We identified a new oscillatory theta-beta component related to the degree of post-error slowing in the correct responses following an erroneous trial. Additionally, we found that the activity of the right dorsolateral prefrontal cortex, the right inferior frontal cortex, and the right superior frontal cortex was correlated with the degree of caution shown in the trial following the commission of an error. Given the overlap between this brain network and the regions activated by the need to inhibit motor responses in a stop-signal manipulation, we conclude that the increase in cognitive control observed after the commission of an error is implemented through the participation of an inhibitory mechanism.

The Effects of COMT (Val108/158Met) and DRD4 (SNP −521) Dopamine Genotypes on Brain Activations Related to Valence and Magnitude of Rewards

Peoples sensitivity to reinforcing stimuli such as monetary gains and losses shows a wide interindividual variation that might in part be determined by genetic differences. Because of the established role of the dopaminergic system in the neural encoding of rewards and negative events, we investigated young healthy volunteers being homozygous for either the Valine or Methionine variant of the catechol-O-methyltransferase (COMT) codon 158 polymorphism as well as homozygous for the C or T variant of the SNP -521 polymorphism of the dopamine D4 receptor. Participants took part in a gambling paradigm featuring unexpectedly high monetary gains and losses in addition to standard gains/losses of expected magnitude while undergoing functional magnetic resonance imaging at 3 T. Valence-related brain activations were seen in the ventral striatum, the anterior cingulate cortex, and the inferior parietal cortex. These activations were modulated by the COMT polymorphism with greater effects for valine/valine participants but not by the D4 receptor polymorphism. By contrast, magnitude-related effects in the anterior insula and the cingulate cortex were modulated by the D4 receptor polymorphism with larger responses for the CC variant. These findings emphasize the differential contribution of genetic variants in the dopaminergic system to various aspects of reward processing.

Genetic Variability in the Dopamine System (Dopamine Receptor D4, Catechol-O-Methyltransferase) Modulates Neurophysiological Responses to Gains and Losses

BACKGROUNDnInterindividual variability in the processing of reward might be partially explained by genetic differences in the dopamine system. Here, we study whether brain responses (event-related potentials [ERPs], oscillatory activity) to monetary gains and losses in normal human subjects are modulated as a function of two dopaminergic polymorphisms (catechol-O-methyltransferase [COMT] valine [Val]158methionine [Met], dopamine receptor D4 [DRD4] single nucleotide polymorphism [SNP] -521).nnnMETHODSnForty participants homozygous for the different alleles of both polymorphisms were selected from a larger population to assess the main effects and interactions. Based on the phasic/tonic dopamine hypothesis, we expected increased brain responses to losses and gains in participants homozygous for the Val/Val variant of the COMT polymorphism (related to higher enzyme activity).nnnRESULTSnThe medial frontal negativity (MFN) of the ERP and the increase in beta power for gains were enhanced for participants homozygous for the COMT ValVal allele when compared with homozygous MetMet participants. In contrast, no modulations in gain- and loss-related brain activity were found to be a function of the DRD4 SNP -521 polymorphism.nnnCONCLUSIONSnThe results demonstrate the role of the COMT Val/Met polymorphism in the processing of reward, consistent with theoretical explanations that suggest the possible role of dopamine in the MFN and beta power increase generation. In addition, the present results might agree with the phasic/tonic dopamine theory that predicts higher phasic dopamine responses in ValVal participants.

Brain activations reflect individual discount rates in intertemporal choice

Humans discount the value of future rewards following a hyperbolic function and thus may prefer a smaller immediate reward over a larger delayed reward. Marked interindividual differences in the steepness of this discounting function can be observed which can be quantified by the parameter k of the discount function. Here, we asked how differences in delay discounting behaviour are reflected by brain activation patterns. Sixteen healthy participants were studied in a slow event-related functional magnetic resonance imaging experiment at 3T. In each trial, participants had to decide between a smaller but immediately available monetary reward (ranging between 14 and 84 Euro) and a larger delayed reward (26 to 89 Euro; delay 5 to 169days) by button press. Participants had the chance to receive the reward corresponding to one of their decisions at the end of the experiment. As expected, participants differed widely with respect to the steepness of their discount function. By contrasting decisions at or near the individual participants indifference point (as determined by parameter k) with trials either well below or well above this point two different brain networks with opposing activation patterns were revealed: Trials below or above the indifference point were associated with activation in the ventral striatum and ventromedial prefrontal cortex, whereas decisions at the indifference point gave rise to activation in medial prefrontal cortex. The opposite effects in the two systems at individual indifference point were interpreted as a reflection of response conflict.

Functional neural dynamics underlying auditory event-related N1 and N1 suppression response

Presenting tone triplets of identical stimuli preceded by silent intervals of 30 s produces a series of three N1 averaged event-related potentials (ERPs), the first being of greater amplitude (non-suppressed N1) than the second and third ones (suppressed N1). Maximal statistically independent components (ICs) of single-trial multi-electrode scalp EEG responses to triplets were obtained by ICA algorithm, and then each IC was searched for underlying brain structures by LORETA inverse solution, and for oscillatory contributions by time-frequency analysis. Non-suppressed N1 cortical mechanisms were broken down into five ICs, grouped in two time-windows (early-onset and late-onset) involving the participation of temporal, frontal and parietal structures, and sub-serving EEG oscillatory contributions of power enhancement and putative phase concentration of mainly theta, alpha and low beta bands. Suppressed N1 was due to the modulation of two above-mentioned early-onset ICs, involving temporal structures only, and mainly sub-serving oscillatory contributions of phase concentration of theta and alpha. Present results, showing quantifiable changes of IC descriptors - i.e. time window of activation, implied structures and oscillatory contributions - extracted from two distinct brain functional situations (non-suppressed versus suppressed N1), give support to the view that ICA is not merely a statistical latent variables model when applied to ERPs, but could help to capture underlying specific function subunits of brain dynamics.

Wavelet analysis of the EEG during the neurocognitive evaluation of invalidly cued targets.

In a spatial central cueing paradigm, positions in the horizontal meridian were cued to evaluate the neurocognitive processing of validly (V) and invalidly cued (I) targets. ERPs were obtained from 20 EEG channel recordings. Complex Morlet wavelets were applied for computing event-related spectral power (ERSP) modulations and inter-trial phase coherence (ITC). P3a and P3b responses were increased in a statistically significant manner in I targets with regard to V targets. This increase seems to be generated only by phase resetting without enhancement of spectral power. Comparing ERSP modulations between I and V target trials we found a major effect centred in the alpha range. The following results were obtained for invalid condition in relation to valid condition: 6-12Hz ERSP decrease topographically widespread over the scalp, starting around 450 ms and peaking around 650 ms; 10-14Hz ERSP increase peaking around 200 ms at fronto-central electrodes; and 10-14Hz ERSP decrease occurring from 400 to 600 ms at posterior electrodes. Therefore, the invalidity effect indeed produces salient changes in the stimulus related and ongoing neuronal activity leading to a brain state of comparative higher activity both excitatory and inhibitory with respect to the validly cued target processing.

Complex networks in brain electrical activity

This letter reports a method to extract a functional network of the human brain from electroencephalogram measurements. A network analysis was performed on the resultant network and the statistics of the cluster coefficient, node degree, path length, and physical distance of the links, were studied. Even given the low electrode count of the experimental data the method was able to extract networks with network parameters that clearly depend on the type of stimulus presented to the subject. This type of analysis opens a door to studying the cerebral networks underlying brain electrical activity, and links the fields of complex networks and cognitive neuroscience.