Tonic–Phasic Dopamine Regulatory Restoration in Psychosis

Description This record contains the manuscript: “Dynamical Systems Model of Tonic–Phasic Dopamine Regulatory Restoration in Psychosis. ” The work introduces a dynamical systems framework describing the maintenance of psychosis through the regulatory interaction between tonic dopaminergic baseline signaling and phasic dopaminergic prediction-error responses. Rather than treating dopaminergic dysregulation as a static increase in dopamine concentration, the model formalizes psychosis as a regulatory gain instability that emerges when phasic dopaminergic signaling exceeds tonic regulatory capacity. The framework integrates tonic dopamine baseline, phasic burst signaling, attentional amplification, and environmental stimulus input within a coupled dynamical system operating on a seconds-to-minutes timescale relevant to salience attribution and symptom maintenance. Core Dynamical System The regulatory dynamics are described by the following coupled equations. Tonic dopamine dynamics: dTD/dt = ρ − λTD − κΦD − σS Phasic dopamine response to stimuli: ΦD (t) = ξ · Sₜ (t) · (1 + γAₜ (t) ) Attentional reinforcement dynamics: dAₜ/dt = ηΦD − μAₜ Environmental stimulus input is modeled as a stochastic process: Sₜ (t) ~ Normal (μₛ, σₛ²) Interpretation of Dopaminergic Excess Within this framework, the dopaminergic excess frequently observed in psychosis is interpreted as a regulatory imbalance between tonic baseline dopamine and phasic dopamine signaling, rather than as a simple increase in absolute dopamine concentration. Biological mechanisms that increase dopamine signaling—such as increased synthesis, reduced reuptake, or vesicular storage expansion—are represented by increases in the phasic sensitivity parameter ξ, which amplifies phasic dopamine responses ΦD. Simultaneously, tonic dopaminergic baseline TD may decline through metabolic decay (λTD), stress input (σS), or depletion associated with repeated phasic activation (κΦD). The combined effect increases the effective gain of dopaminergic signaling. Salience Gain Instability Principle The regulatory balance between tonic and phasic dopamine is captured by the Salience Gain Ratio: G = ΦD / TD Psychotic instability occurs when: ΦD / TD > θ where θ represents the cortical gating threshold associated with prefrontal inhibitory control. This boundary acts as a separatrix in phase space, dividing trajectories that converge toward stable regulatory dynamics from those that diverge toward a runaway salience attractor. When this instability occurs, neutral stimuli may acquire abnormal significance, producing persistent aberrant salience attribution. Stability Conditions Local stability of attentional dynamics requires: η ξ γ Sₜ κΦD + σS Violation of these conditions drives the system into a Salience Gain Instability Region. Empirical Predictions The model generates several testable predictions: • Psychotic symptom severity correlates with the salience gain ratio G = ΦD / TD• Restoring tonic dopaminergic baseline should reduce aberrant salience without impairing reward learning• Acute stress inputs may shift the system equilibrium across the instability boundary• Pharmacological suppression of phasic signaling stabilizes the system but may reduce motivational function Scope The framework models the maintenance dynamics of positive psychotic symptoms associated with dopaminergic dysregulation rather than the developmental etiology of schizophrenia. Tonic and phasic dopamine are treated as latent regulatory variables inferred from neuroimaging and behavioral proxies. Author Evangelos-Konstantinos GeorgantasIndependent ResearcherGreece