# A Computational Model for the Simulation of Prepulse Inhibition and Its Modulation by Cortical and Subcortical Units

## TL;DR

This paper presents a computational model to simulate how brain circuits control a reflex called prepulse inhibition, which is linked to nervous system function.

## Contribution

The study introduces a novel computational model that integrates brainstem and modulatory cortical/subcortical units to simulate prepulse inhibition.

## Key findings

- The model replicates key experimental features of prepulse inhibition, including effects of stimulus timing and intensity.
- Simulations show that subcortical units are central to modulating prepulse inhibition.
- Drug simulations demonstrate how GABAergic and dopaminergic agents impair prepulse inhibition.

## Abstract

The sensorimotor gating is a nervous system function that modulates the acoustic startle response (ASR). Prepulse inhibition (PPI) phenomenon is an operational measure of sensorimotor gating, defined as the reduction of ASR when a high intensity sound (pulse) is preceded in milliseconds by a weaker stimulus (prepulse). Brainstem nuclei are associated with the mediation of ASR and PPI, whereas cortical and subcortical regions are associated with their modulation. However, it is still unclear how the modulatory units can influence PPI. In the present work, we developed a computational model of a neural circuit involved in the mediation (brainstem units) and modulation (cortical and subcortical units) of ASR and PPI. The activities of all units were modeled by the leaky-integrator formalism for neural population. The model reproduces basic features of PPI observed in experiments, such as the effects of changes in interstimulus interval, prepulse intensity, and habituation of ASR. The simulation of GABAergic and dopaminergic drugs impaired PPI by their effects over subcortical units activity. The results show that subcortical units constitute a central hub for PPI modulation. The presented computational model offers a valuable tool to investigate the neurobiology associated with disorder-related impairments in PPI.