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Toward Translational Mechanisms of Learned Helplessness: Linking Behavior, Computation, and Neural Modulation

Poster Session D - Monday, March 9, 2026, 8:00 – 10:00 am PDT, Fairview/Kitsilano Ballroom

Adithya Anil¹ (), Arjun Ramakrishnan²; ¹Indian Institute of Technology Kanpur

Motivational deficits are a hallmark of depression, yet their underlying mechanisms remain unclear. Within the Research Domain Criteria (RDoC) framework, learned helplessness (LH) provides a model for these impairments, displaying passivity even when control is possible. Such passivity may arise from an overactive Pavlovian system that biases behavior toward punishment-aversive inaction (Pavlovian bias). Or it could be due to weakened drive to act (action bias) which would also manifest as reduced choice stochasticity—reflecting diminished exploration and increased behavioral rigidity – under uncertainty. We tested these hypotheses using a modified Levine task to induce helplessness through solvable (control) or unsolvable (experimental) conditions. Participants (N = 112; 74 retained: 35 control, 39 experimental) completed an orthogonalized Go/No-Go (o-GNG) task before and after induction, dissociating Pavlovian and instrumental components. Behavioral indices and hierarchical Bayesian modeling (HBayesDM) parameters quantified latent constructs of action bias, Pavlovian bias, and choice stochasticity. Modeling supported the action bias hypothesis: we observed a significant reduction in action bias (pre: 1.55, post: 0.61; HDI (post-pre) = [−1.8, −0.1]) and choice stochasticity (pre: 0.14, post: 0.04; HDI (post-pre) = [−0.2, −0.02]) following helplessness induction, indicating diminished drive to act and reduced exploration. Furthermore, experimental group participants with elevated depressive symptoms (PHQ-9 ≥ 8; n = 14) showed nearly double the decline in action bias. On the other hand, Pavlovian bias remained stable. These findings highlight reduced action vigor and exploration as key computational features linking helplessness to depressive symptomatology and highlight a potential target for dACC–dlPFC modulation.

Topic Area: THINKING: Decision making