Journal
COGNITIVE NEURODYNAMICS
Volume -, Issue -, Pages -Publisher
SPRINGER
DOI: 10.1007/s11571-023-09999
Keywords
Obsessive-compulsive disorder; Dopamine; Computational model; Working memory; Prefrontal cortex
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This study establishes a biophysical model to explain the mechanism of how high dopamine concentrations induce persistent neuronal activities and working memory defects, leading to obsession and compulsion. The theory highlights the importance of early intervention and behavioral therapies for obsessive-compulsive disorder, offering new approaches to dopaminergic pharmacotherapy and psychotherapy.
Dopamine modulates working memory in the prefrontal cortex (PFC) and is crucial for obsessive-compulsive disorder (OCD). However, the mechanism is unclear. Here we establish a biophysical model of the effect of dopamine (DA) in PFC to explain the mechanism of how high dopamine concentrations induce persistent neuronal activities with the network plunging into a deep, stable attractor state. The state develops a defect in working memory and tends to obsession and compulsion. Weakening the reuptake of dopamine acts on synaptic plasticity according to Hebbian learning rules and reward learning, which in turn affects the strength of neuronal synaptic connections, resulting in the tendency of compulsion and learned obsession. In addition, we elucidate the potential mechanisms of dopamine antagonists in OCD, indicating that dopaminergic drugs might be available for treatment, even if the abnormality is a consequence of glutamate hypermetabolism rather than dopamine. The theory highlights the significance of early intervention and behavioural therapies for obsessive-compulsive disorder. It potentially offers new approaches to dopaminergic pharmacotherapy and psychotherapy for OCD patients.
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