# Computational insights on asymmetrical D1 and D2 receptor-mediated chunking: implications for OCD and Schizophrenia

## TL;DR

This paper explores how differences in dopamine receptor activity might influence repetitive behaviors in OCD and schizophrenia using a computational model.

## Contribution

The study introduces a computational model showing how asymmetrical D1 and D2 receptor interactions affect chunking and start/stop signaling.

## Key findings

- Asymmetric intra-network connections and synaptic weights influence start/stop signaling in learned sequences.
- Differential time constants between D1 and D2 populations contribute to chunk boundary signaling.
- Larger circuit dynamics, not just striatal connections, support start and stop dichotomies.

## Abstract

Repetitive thoughts and motor programs including perseveration are bridge symptoms characteristic of obsessive compulsive disorder (OCD), schizophrenia and in the co-morbid overlap of these conditions. The above pathologies are sensitive to altered activation and kinetics of dopamine \documentclass[12pt]{minimal}
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\begin{document}$$D_{2}$$\end{document}D2 receptors that differently influence sequence learning and recall. Recognizing start and stop elements of motor and cognitive behaviors has crucial importance. During chunking, frequent components of temporal strings are concatenated into single units. We extended a published computational model (Asabuki et al. 2018), where two populations of neurons are connected and simulated in a reservoir computing framework. These neural pools were adopted to represent D1 and D2 striatal neuronal populations. We investigated how specific neural and striatal circuit parameters can influence start/stop signaling and found that asymmetric intra-network connection probabilities, synaptic weights and differential time constants may contribute to signaling of start/stop elements within learned sequences. Asymmetric coupling between the striatal \documentclass[12pt]{minimal}
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\begin{document}$$D_{2}$$\end{document}D2 neural populations was also demonstrated to be beneficial. Our modeling results predict that dynamical differences between the two dopaminergic striatal populations and the interaction between them may play complementary roles in chunk boundary signaling. Start and stop dichotomies can arise from the larger circuit dynamics as well, since neural and intra-striatal connections only partially support a clear division of labor.