Memories are gradually consolidated after initial encoding, and this can sometimes lead to a transition from implicit to explicit knowledge. The exact physiological processes underlying this reorganization remain unclear. Here, we used a serial reaction time task to determine whether targeted memory reactivation (TMR) of specific memory traces during slow-wave sleep promotes the emergence of explicit knowledge. Human participants learned two 12-item sequences of button presses (A and B). These differed in both cue order and in the auditory tones associated with each of the four fingers (one sequence had four higher-pitched tones). Subsequent overnight sleep was monitored, and the tones associated with one learned sequence were replayed during slow-wave sleep. After waking, participants demonstrated greater explicit knowledge (p = 0.005) and more improved procedural skill (p = 0.04) for the cued sequence relative to the uncued sequence. Furthermore, fast spindles (13.5–15 Hz) at task-related motor regions predicted overnight enhancement in procedural skill (r = 0.71, p = 0.01). Auditory cues had no effect on post-sleep memory performance in a control group who received TMR before sleep. These findings suggest that TMR during sleep can alter memory representations and promote the emergence of explicit knowledge, supporting the notion that reactivation during sleep is a key mechanism in this process.
consolidation; explicit memory; learning; reactivation; replay; slow-wave sleep
Some people perceive themselves to look more, or less attractive than they are in reality. We investigated the role of emotions in enhancement and derogation effects; specifically, whether the propensity to experience positive and negative emotions affects how healthy we perceive our own face to look and how we judge ourselves against others. A psychophysical method was used to measure healthiness of self-image and social comparisons of healthiness. Participants who self-reported high positive (N = 20) or negative affectivity (N = 20) judged themselves against healthy (red-tinged) and unhealthy looking (green-tinged) versions of their own and stranger’s faces. An adaptive staircase procedure was used to measure perceptual thresholds. Participants high in positive affectivity were un-biased in their face health judgement. Participants high in negative affectivity on the other hand, judged themselves as equivalent to less healthy looking versions of their own face and a stranger’s face. Affective traits modulated self-image and social comparisons of healthiness. Face health judgement was also related to physical symptom perception and self-esteem; high physical symptom reports were associated a less healthy self-image and high self-reported (but not implicit) self-esteem was associated with more favourable social comparisons of healthiness. Subject to further validation, our novel face health judgement task could have utility as a perceptual measure of well-being. We are currently investigating whether face health judgement is sensitive to laboratory manipulations of mood.
Bipolar disorder is characterized by impaired decision-making captured in impulsivity and risk-taking. We sought to determine whether this is driven by a failure to effectively weight the lower-order goal of obtaining a strongly desired reward in relation to higher-order goals, and how this relates to trait impulsivity and risk-taking. We hypothesized that in bipolar disorder the weighting of valuation signals converging on ventromedial prefrontal cortex are more heavily weighted towards ventral striatum inputs (lower-order), with less weighting of dorsolateral prefrontal cortex inputs (higher-order). Twenty euthymic patients with bipolar disorder not in receipt of antipsychotic medication and 20 case-matched controls performed a roulette task during functional magnetic resonance imaging. Activity in response to high-probability (‘safe’) and low-probability (‘risky’) prospects was measured during both anticipation, and outcome. In control subjects, anticipatory and outcome-locked activity in dorsolateral prefrontal cortex was greater for safe than risky reward prospects. The bipolar disorder group showed the opposite pattern with preferential response to risky rewards. This group also showed increased anticipatory and outcome-locked activity in ventral striatum in response to rewards. In control subjects, however, ventromedial prefrontal activation was positively associated with both ventral striatum and dorsolateral prefrontal activity; patients evidenced a strong positive association with ventral striatum, but a negative association with dorsolateral prefrontal cortex. Response to high-probability rewards in dorsolateral prefrontal cortex was inversely associated with trait impulsivity and risk-taking in the bipolar disorder group. Our findings suggest that clinically impulsive and risky decision-making are related to subjective valuation that is biased towards lower-order preference, with diminished integration of higher-order goals. The findings extend a functional neuroanatomical account of disorders characterized by clinically impulsive decision-making, and provide targets for evaluating interventions that foster self-control.
bipolar disorder; mania; reward; striatum; accumbens; risk
•People may use Bayesian inference to update their own self-representation.•Self- and other-representations may help predict outcomes of social interactions.•The value of an outcome is essentially the prior belief that it can be achieved.•‘Active inference’ uses free-energy-minimization to achieve desirable outcomes.•A positive self-representation may be a desirable outcome of active inference.
Viewing the brain as an organ of approximate Bayesian inference can help us understand how it represents the self. We suggest that inferred representations of the self have a normative function: to predict and optimise the likely outcomes of social interactions. Technically, we cast this predict-and-optimise as maximising the chance of favourable outcomes through active inference. Here the utility of outcomes can be conceptualised as prior beliefs about final states. Actions based on interpersonal representations can therefore be understood as minimising surprise – under the prior belief that one will end up in states with high utility. Interpersonal representations thus serve to render interactions more predictable, while the affective valence of interpersonal inference renders self-perception evaluative. Distortions of self-representation contribute to major psychiatric disorders such as depression, personality disorder and paranoia. The approach we review may therefore operationalise the study of interpersonal representations in pathological states.
Self-representation; Other-representation; Free energy minimisation; Active inference; Personality disorder; Paranoia
Introduction: We propose that active Bayesian inference—a general framework for decision-making—can equally be applied to interpersonal exchanges. Social cognition, however, entails special challenges. We address these challenges through a novel formulation of a formal model and demonstrate its psychological significance.
Method: We review relevant literature, especially with regards to interpersonal representations, formulate a mathematical model and present a simulation study. The model accommodates normative models from utility theory and places them within the broader setting of Bayesian inference. Crucially, we endow people's prior beliefs, into which utilities are absorbed, with preferences of self and others. The simulation illustrates the model's dynamics and furnishes elementary predictions of the theory.
Results: (1) Because beliefs about self and others inform both the desirability and plausibility of outcomes, in this framework interpersonal representations become beliefs that have to be actively inferred. This inference, akin to “mentalizing” in the psychological literature, is based upon the outcomes of interpersonal exchanges. (2) We show how some well-known social-psychological phenomena (e.g., self-serving biases) can be explained in terms of active interpersonal inference. (3) Mentalizing naturally entails Bayesian updating of how people value social outcomes. Crucially this includes inference about one's own qualities and preferences.
Conclusion: We inaugurate a Bayes optimal framework for modeling intersubject variability in mentalizing during interpersonal exchanges. Here, interpersonal representations are endowed with explicit functional and affective properties. We suggest the active inference framework lends itself to the study of psychiatric conditions where mentalizing is distorted.
free energy; active inference; value; evidence; surprise; self-organization; interpersonal; Bayesian
Volume conduction (VC) and magnetic field spread (MFS) induce spurious correlations between EEG/MEG sensors, such that the estimation of functional networks from scalp recordings is inaccurate. Imaginary coherency  reduces VC/MFS artefacts between sensors by assuming that instantaneous interactions are caused predominantly by VC/MFS and do not contribute to the imaginary part of the cross-spectral densities (CSDs). We propose an adaptation of the dynamic imaging of coherent sources (DICS)  - a method for reconstructing the CSDs between sources, and subsequently inferring functional connectivity based on coherences between those sources. Firstly, we reformulate the principle of imaginary coherency by performing an eigenvector decomposition of the imaginary part of the CSD to estimate the power that only contributes to the non-zero phase-lagged (NZPL) interactions. Secondly, we construct an NZPL-optimised spatial filter with two a priori assumptions: (1) that only NZPL interactions exist at the source level and (2) the NZPL CSD at the sensor level is a good approximation of the projected source NZPL CSDs. We compare the performance of the NZPL method to the standard method by reconstructing a coherent network from simulated EEG/MEG recordings. We demonstrate that, as long as there are phase differences between the sources, the NZPL method reliably detects the underlying networks from EEG and MEG. We show that the method is also robust to very small phase lags, noise from phase jitter, and is less sensitive to regularisation parameters. The method is applied to a human dataset to infer parts of a coherent network underpinning face recognition.
The lack of clear understanding of the pathophysiology of chronic pain could explain why we currently have only a few effective treatments. Understanding how pain relief is realised during placebo analgesia could help develop improved treatments for chronic pain. Here, we tested whether experimental placebo analgesia was associated with altered resting-state cortical activity in the alpha frequency band of the electroencephalogram (EEG). Alpha oscillations have been shown to be influenced by top-down processes, which are thought to underpin the placebo response.
Seventy-three healthy volunteers, split into placebo or control groups, took part in a well-established experimental placebo procedure involving treatment with a sham analgesic cream. We recorded ongoing (resting) EEG activity before, during, and after the sham treatment.
We show that resting alpha activity is modified by placebo analgesia. Post-treatment, alpha activity increased significantly in the placebo group only (p < 0.001). Source analysis suggested that this alpha activity might have been generated in medial components of the pain network, including dorsal anterior cingulate cortex, medial prefrontal cortex, and left insula.
These changes are consistent with a cognitive state of pain expectancy, a key driver of the placebo analgesic response. The manipulation of alpha activity may therefore present an exciting avenue for the development of treatments that directly alter endogenous processes to better control pain.
The electrically-evoked compound action potential (ECAP) is the synchronous whole auditory nerve activity in response to an electrical stimulus, and can be recorded in situ on cochlear implant (CI) electrodes. A novel procedure (ECAP-ICA) to isolate the ECAP from the stimulation artifact, based on independent component analysis (ICA), is described here. ECAPs with artifact (raw-ECAPs) were sequentially recorded for the same stimulus on 9 different intracochlear recording electrodes. The raw-ECAPs were fed to ICA, which separated them into independent sources. Restricting the ICA projection to 4 independent components did not induce under-fitting and was found to explain most of the raw-data variance. The sources were identified and only the source corresponding to the neural response was retained for artifact-free ECAP reconstruction. The validity of the ECAP-ICA procedure was supported as follows: N1 and P1 peaks occurred at usual latencies; and ECAP-ICA and artifact amplitude-growth functions (AGFs) had different slopes. Concatenation of raw-ECAPs from multiple stimulus currents, including some below the ECAP-ICA threshold, improved the source separation process. The main advantage of ECAP-ICA is that use of maskers or alternating polarity stimulation are not needed.
•Novel technique to cancel artifact in electrically-evoked compound action potentials.•No maskers or alternate polarity are required.•ECAPs output from the procedure are compared to forward-masking technique.
AN, auditory nerve; CI, cochlear implant; CI24RE, Cochlear® Nucleus Freedom™ cochlear implant – 22 active electrodes and 2 ground electrodes; ECAP, electrically-evoked compound action potential; ECAP-FM, ECAP obtained with the forward-masking technique; ECAP-ICA, ECAP obtained with the ICA artifact rejection technique; ICA, independent component analysis; IC, independent component (or source); JADE-R, joint approximate diagonalisation of the cross-cumulants eigenmatrices (computational implementation of ICA); MP1, extracochlear ground electrode; MP2, ground electrode placed on the case of the cochlear implant; N1P1, peak-to-peak voltage difference measurement of ECAP amplitude; RMS, root mean square; SNR, signal to noise ratio
Mania is characterised by increased impulsivity and risk-taking, and psychological accounts argue that these features may be due to hypersensitivity to reward. The neurobiological mechanisms remain poorly understood. Here we examine reinforcement learning and sensitivity to both reward and punishment outcomes in hypomania-prone individuals not receiving pharmacotherapy.
We recorded EEG from 45 healthy individuals split into three groups by low, intermediate and high self-reported hypomanic traits. Participants played a computerised card game in which they learned the reward contingencies of three cues. Neural responses to monetary gain and loss were measured using the feedback-related negativity (FRN), a component implicated in motivational outcome evaluation and reinforcement learning.
As predicted, rewards elicited a smaller FRN in the hypomania-prone group relative to the low hypomania group, indicative of greater reward responsiveness. The hypomania-prone group also showed smaller FRN to losses, indicating diminished response to negative feedback.
Our findings indicate that proneness to hypomania is associated with both reward hypersensitivity and discounting of punishment. This positive evaluation bias may be driven by aberrant reinforcement learning signals, which fail to update future expectations. This provides a possible neural mechanism explaining risk-taking and impaired reinforcement learning in BD. Further research will be needed to explore the potential value of the FRN as a biological vulnerability marker for mania and pathological risk-taking.
The therapeutic response to a drug treatment is a mixture of direct pharmacological action and placebo effect. Therefore, harnessing the positive aspects of the placebo effect and reducing the negative ones could potentially benefit the patient. This article is aimed at providing an overview for clinicians of the importance of contextual psychosocial variables in determining treatment response, and the specific focus is on determinants of the placebo response. A better understanding of the physiological, psychological, and social mechanisms of placebo may aid in predicting which contexts have the greatest potential for inducing positive treatment responses. We examine the evidence for the role of psychological traits, including optimism, pessimism, and the effect of patient expectations on therapeutic outcome. We discuss the importance of the patient-practitioner relationship and how this can be used to enhance the placebo effect, and we consider the ethical challenges of using placebos in clinical practice.
Attention can be directed to particular spatial locations, or to objects that appear at anticipated points in time. While most work has focused on spatial or temporal attention in isolation, we investigated covert tracking of smoothly moving objects, which requires continuous coordination of both. We tested two propositions about the neural and cognitive basis of this operation: first that covert tracking is a right hemisphere function, and second that pre-motor components of the oculomotor system are responsible for driving covert spatial attention during tracking. We simultaneously recorded event related potentials (ERPs) and eye position while participants covertly tracked dots that moved leftward or rightward at 12 or 20°/s. ERPs were sensitive to the direction of target motion. Topographic development in the leftward motion was a mirror image of the rightward motion, suggesting that both hemispheres contribute equally to covert tracking. Small shifts in eye position were also lateralized according to the direction of target motion, implying covert activation of the oculomotor system. The data addresses two outstanding questions about the nature of visuospatial tracking. First, covert tracking is reliant upon a symmetrical frontoparietal attentional system, rather than being right lateralized. Second, this same system controls both pursuit eye movements and covert tracking.
Schizophrenia is currently diagnosed on the basis of patient reports and clinical observations. A diagnosis based on aetiology is inherently more reliable due to being closer to the disease process than the overt clinical manifestations. Accordingly, recent research in schizophrenia has focused on the development of biomarkers in a bit to improve the reliability and neurobiological relevance of the diagnosis. Visual information processing is one of these promising fields of recent biomarker research.
This article provides an overview of the available literature regarding deficits in schizophrenia detectable through psychophysical (contrast and motion sensitivity, visual backward-masking), ERP (P1 and N1 visual evoked potentials) and oscillatory (signal power and phase-locking factor of evoked oscilations) measures and their validity as trait or state biomarkers of the disease. The methodology included a search on articles related to visual information processing in schizophrenia on the PubMed database.
Biomarker research in schizophrenia is a rapidly expanding area. Evidence exists to suggest that both psychotic and manic symptoms are associated with visual processing abnormalities. A specific impairment confined to the magnocellular component of the visual system might be a trait biomarker of schizophrenia.
schizophrenia; diagnosis; early detection; trait biomarkers; state biomarkers; P1; oscillations; magnocellular pathway
The neural mechanisms whereby placebo conditioning leads to placebo analgesia remain unclear. In this study we aimed to identify the brain structures activated during placebo conditioning and subsequent placebo analgesia. We induced placebo analgesia by associating a sham treatment with pain reduction and used fMRI to measure brain activity associated with three stages of the placebo response: before, during and after the sham treatment, while participants anticipated and experienced brief laser pain. In the control session participants were explicitly told that the treatment was inactive. The sham treatment group reported a significant reduction in pain rating (p = 0.012). Anticipatory brain activity was modulated during placebo conditioning in a fronto-cingulate network involving the left dorsolateral prefrontal cortex (DLPFC), medial frontal cortex and the anterior mid-cingulate cortex (aMCC). Identical areas were modulated during anticipation in the placebo analgesia phase with the addition of the orbitofrontal cortex (OFC). However, during altered pain experience only aMCC, post-central gyrus and posterior cingulate demonstrated altered activity. The common frontal cortical areas modulated during anticipation in both the placebo conditioning and placebo analgesia phases have previously been implicated in placebo analgesia. Our results suggest that the main effect of placebo arises from the reduction of anticipation of pain during placebo conditioning that is subsequently maintained during placebo analgesia.
Placebo analgesia; Placebo; fMRI; Laser; Conditioning