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Price, T. A.

Publications and source records attributed to Price, T. A..

4 recordsLinked to original sources

Low-dimensional factorized neural computations underlie risk-adaptive choices

Real-world decision-making rarely occurs with perfect information. Instead, individuals must constantly weigh potential rewards against the probability of adverse outcomes.1 Failures of this process can lead to maladaptive decisions associated with reduced lifetime success, and numerous psychiatric disorders such as gambling addictions, bulimia nervosa, and substance use disorder.2,3 The neural computations that facilitate inference about the landscape of potential outcomes remain unclear, but are thought to occur in distributed frontotemporal circuits.4 Here we used deep reinforcement learning agents to predict distinct behavioral strategies and their underlying neural population dynamics during a risky decision-making task. Across a range of training conditions, deep reinforcement learning agents separated into strategies marked by either overly cautious exploration of the reward contingency space or a high-performing, risk-adaptive Bimodal strategy. The internal dynamics of high-performing Bimodal agents formed low-dimensional representations that segregated safe and risky states. In contrast, the cautious exploration agents were associated with more skewed and entangled neural representations. We found remarkably similar dynamical representations and their associated behavioral strategies in neuronal ensemble recordings from human epilepsy patients performing a similar risky decision-making task. These results reveal the structure of dynamical computations that underlie inferences about uncertain outcomes and their associated behavioral strategies.

neuroscience↗

Temporal Processing during Decision Making under Uncertainty.

Time perception and decision-making are interrelated processes that are critical to much of human and animal behavior. Although the behavioral importance of this link between the processes has been established, the neural underpinnings of temporal decision-making are unclear. The current study leverages human intracranial electro-physiology to investigate the neural contribution of temporal processing to decision-making under risk. To probe temporal decision-making, we use a version of the Balloon Analogue Risk Task, in which participants inflate virtual balloons with the goal of reaching maximal balloon size but stopping inflation before the balloon pops. Points are awarded based on inflation duration of successful trials, such that points awarded are linearly related to balloon size. By decoding temporal features of the task on a trial-by-trial basis, we find neural representations of time during balloon inflation. Specifically, we find that both medial and lateral temporal regions of the brain encode the majority of this time-related signal. Importantly, we can decode the progression of time leading up to the outcome of a successful decision (pressing a button to stop inflation before the balloon pops). This encoding of time depends on an active decision to end the trial: we cannot decode time during passive observation of balloon inflation to a known maximal size. To validate these results further, we use a temporal convolution network to predict participants response (i.e., time of button press) based on the brain activity leading up to the response. We find that we can predict the moment of response with high accuracy and temporal resolution. The model predicts the timing of successful decisions but not the timing of balloon pops. Together, these findings reveal neural representations that encode the progression of time, specifically in relation to an active decision.

neuroscience↗

Asymmetric Reinforcement Learning Explains Human Choice Patterns in Decision-making Under Risk

Human decisions under uncertainty are shaped by experience, but the computations that translate expectation and experience into choice remain debated in neural and cognitive science. Prior studies highlight reinforcement learning (RL) as a unifying framework, yet it is unclear whether human behavior under risk is better captured by symmetric updating from outcomes or by asymmetric learning that weights reward and loss differently. This work examines which learning strategies better explain trial-by-trial choices given contextual uncertainty and manipulations of outcome distributions. Our results show that a Risk Sensitive (RS) model with asymmetric learning rates best explains human behavior in our novel decision-making task. Fitting candidate models to individual trial histories yielded value signals that predicted both choice and response time. These results highlight that RS model, as an asymmetric learning provides a concise and identifiable account of behavior in decision-making under risk tasks.

neuroscience↗

Increased Aperiodic Exponents Track Depression Symptom Severity

Roughly one-third of patients with major depressive disorder (MDD) fail to respond to standard treatments and develop treatment-resistant MDD. For these patients, alternative therapies ofer additional options but yield inconsistent outcomes. Progress has been limited by the absence of objective, brain-based biomarkers to guide target selection or track therapeutic response in real time. Instead, clinicians rely on behavioral assessments that evolve slowly over weeks to months, obscuring the underlying neural dynamics of symptom changes. Here, we test whether the aperiodic exponent of intracranial EEG (iEEG) local field potentials can serve as a neurophysiological marker of depression symptom severity. We leveraged a large iEEG cohort (N = 20) undergoing invasive monitoring for refractory epilepsy, yielding over 1,800 contacts spanning cortical and subcortical zones. For each contact, we estimated the aperiodic exponent (thought to reflect aspects of cortical excitability) of the power spectrum across 10-100 Hz within local brain regions and across distributed cortical association networks. Depressive symptoms were assessed with the Beck Depression Inventory-II (BDI-II) immediately before intracranial resting state recordings. With respect to the BDI-II scale, participants were identified as experiencing minimal (BDI-II [≤] 13) or elevated depression symptoms (BDI-II [≥] 14). Associations between symptom severity (BDI-II total score and Somatic-Afective, Cognitive, and Anhedonia subscales) and region- or network-level exponents were modeled with ordinary least squares (OLS) regression. The whole-brain, mean aperiodic exponent for each participant discriminated symptom status (AUC = 0.82). At the regional level, the orbitofrontal cortex, anterior cingulate cortex, insula, and amygdala showed higher exponents in the elevated depression symptom group (d = 1.18-1.71; p = 0.032-0.004). A post-hoc classification analysis across these four regions misclassified one participant per group (AUC = 0.86; 95% CI 0.64-1.00). In continuous analyses, BDI-II scores correlated positively with exponents in these same four regions (pFDR = 0.019-0.027; partial r=0.61-0.70) and at the network level in the Salience network (pFDR = 0.024; partial r = 0.63) and Default (pFDR = 0.046; partial r = 0.55) network. The Salience network significantly tracked Anhedonia symptoms (p = 0.004; partial r = 0.62). Here we report that intracranial aperiodic exponents within fronto-limbic and insular circuits, overlapping with networks implicated in contemporary accounts of depression pathophysiology, diferentiate depressive symptom status and scale with severity. These findings support the aperiodic exponent as a candidate neurophysiological marker of current depression symptom burden, with potential relevance for individualized neuromodulation in MDD.

neuroscience↗