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Balasubramani, P. P.

Publications and source records attributed to Balasubramani, P. P..

2 recordsLinked to original sources

Orbitofrontal neuron ensembles contribute to inhibitory control

Stopping, or inhibition, is a form of self-control that is a core part of adaptive behavior. We hypothesize that inhibition commands originate, in part, from the orbitofrontal cortex (OFC). We recorded activity of OFC neurons in macaques performing a stop signal task. Decoding analyses revealed a clear difference in ensemble responses that distinguish successful from failed inhibition that begins after the stop signal and before the stop signal reaction time. We also found a different and unrelated ensemble pattern that distinguishes successful from failed stopping before the beginning of the trial. These signals were distinct from, and orthogonal to, value encoding, which was also observed in these neurons. The timing of the early and late signals was, respectively, consistent with the idea that OFC contributes both proactively and reactively to inhibition. These results support the view, inspired by anatomy, that OFC gathers diverse sensory inputs to compute early-stage executive signals.

neuroscience

Bipolar oscillations between positive and negative mood states in a computational model of Basal Ganglia

Bipolar disorder is characterized by mood swings - oscillations between manic and depressive states. The swings (oscillations) mark the length of an episode in a patients mood cycle (period), and can vary from hours to years. The proposed modeling study uses decision making framework to investigate the role of basal ganglia network in generating bipolar oscillations. In this model, the basal ganglia system performs a two-arm bandit task in which one of the arms leads to a positive outcome, while the other leads to a negative outcome. In healthy conditions, the model chooses positive action and avoids negative one, whereas under bipolar conditions, the model exhibits slow oscillations in its choice of positive or negative outcomes, reminiscent of bipolar oscillations. The model is cast at three levels of abstraction: 1) a two-dimensional dynamical system model, 2) a phenomenological basal ganglia model, 3) a detailed network model of basal ganglia. Phase-plane analyses on the simple reduced dynamical system with two variables reveal the essential parameters that generate pathological bipolar-like oscillations. Phenomenological and network models of the basal ganglia extend that logic, and interpret bipolar oscillations in terms of the activity of dopaminergic and serotonergic projections on the cortico-basal ganglia network dynamics. The networks dysfunction, specifically in terms of reward and risk sensitivity, is shown to be responsible for the pathological bipolar oscillations. The study proposes a computational model that explores the effects of impaired serotonergic neuromodulation on the dynamics of the cortico basal ganglia network, and relates this impairment to abstract mood states (manic and depressive episodes) and oscillations of bipolar disorder.

neuroscience