Simulated Dopamine Modulation of a Neurorobotic Model of the Basal Ganglia

Author:

Prescott Tony J.1ORCID,Montes González Fernando M.2ORCID,Gurney Kevin3,Humphries Mark D.4,Redgrave Peter3

Affiliation:

1. Department of Computer Science, University of Sheffield, Sheffield S10 2TN, UK

2. Departamento de Inteligencia Artificial, Universidad Veracruzana, Veracruz 91090, Mexico

3. Department of Psychology, University of Sheffield, Sheffield S10 2TN, UK

4. School of Psychology, University of Nottingham, Nottingham NG7 2RD, UK

Abstract

The vertebrate basal ganglia play an important role in action selection—the resolution of conflicts between alternative motor programs. The effective operation of basal ganglia circuitry is also known to rely on appropriate levels of the neurotransmitter dopamine. We investigated reducing or increasing the tonic level of simulated dopamine in a prior model of the basal ganglia integrated into a robot control architecture engaged in a foraging task inspired by animal behaviour. The main findings were that progressive reductions in the levels of simulated dopamine caused slowed behaviour and, at low levels, an inability to initiate movement. These states were partially relieved by increased salience levels (stronger sensory/motivational input). Conversely, increased simulated dopamine caused distortion of the robot’s motor acts through partially expressed motor activity relating to losing actions. This could also lead to an increased frequency of behaviour switching. Levels of simulated dopamine that were either significantly lower or higher than baseline could cause a loss of behavioural integration, sometimes leaving the robot in a ‘behavioral trap’. That some analogous traits are observed in animals and humans affected by dopamine dysregulation suggests that robotic models could prove useful in understanding the role of dopamine neurotransmission in basal ganglia function and dysfunction.

Funder

UK Engineering and Physical Sciences Research Council

European Union FET Flagship Human Brain Project

Innovate UK Funding under the UK’s funding guarantee scheme for the EIC Pathfinder project CAVAA

SNII-CONACYT support

Publisher

MDPI AG

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