Date of Award

2026-05-01

Degree Name

Doctor of Philosophy

Department

Computational Science

Advisor(s)

Alexander Friedman

Abstract

This thesis develops and applies high-throughput behavioral assays and analysis pipelines to study how external contingencies and internal state shape rodent decision-making. First, it introduces RECORD (Reward-Cost in Rodent Decision-making), a modular platform that combines 3D-printed arenas, microcontroller-based control, and closed-loop trial structure to deliver graded rewards and costs in a foraging-like environment. RECORD supports scalable data collection across multiple arenas and a software stack for parsing, databasing, and extracting spatiotemporal behavioral features and psychometric choice functions. Using this framework, the thesis quantifies how animals integrate sucrose reward magnitude with aversive light cost, revealing structured individual differences and sex-dependent movement signatures during approach-avoidance decisions, and demonstrates compatibility with neuronal recordings. Second, the thesis uses RECORD to test how acute alcohol consumption perturbs cost-benefit choice. By offering ethanol mixed inversely with sucrose concentrations, we quantify how alcohol availability reshapes psychometric functions, approach rates, and engagement with reward zones. Alcohol altered decision policies most strongly for moderate sucrose-alcohol offers, increased behavioral variability, and produced non-sigmoidal response patterns in a subset of animals, with more pronounced effects in males and measurable changes that persisted into post-alcohol task stages. Finally, the thesis examines endocrine modulation of conflict decision-making through the ghrelin receptor (GHSR). Moderate pharmacological GHSR activation selectively increased cost sensitivity during conflict without comparably altering non-conflict reward seeking, and it changed motor signatures of decision engagement (trajectory curvature, movement vigor, head-body orientation, and hesitation). Circuit-level measurements supported a dose-dependent, non-linear mechanism in which moderate GHSR activation preferentially recruits dorsomedial striosomes and lateral habenula and suppresses downstream dopamine signaling; chemogenetic activation of striosomes was sufficient to recapitulate the cost-sensitive behavioral phenotype. Together, these studies provide a systems-level account of how internal state signals and pharmacological perturbations bias cost-benefit computations, and they establish a generalizable experimental and computational framework for investigating decision-making across health and disease.

Language

en

Provenance

Received from ProQuest

File Size

116 p.

File Format

application/pdf

Rights Holder

Atanu Giri

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