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Motor cortex dysfunction in problem gamblers.

Nahian S Chowdhury¹, Evan J Livesey¹, Alex Blaszczynski¹

¹School of Psychology, The University of Sydney, Camperdown, New South Wales, Australia.

Addiction Biology

|January 14, 2020

Summary

This summary is machine-generated.

Problem gambling is linked to altered brain neurotransmission, specifically weaker GABA_A receptor activity and higher glutamate receptor activity in the primary motor cortex (M1). Poorer response inhibition correlated with reduced M1 GABA_A activity.

Keywords:

GABA glutamate impulsivity problem gambling response inhibition transcranial magnetic stimulation

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Area of Science:

Neuroscience
Psychiatry
Neurophysiology

Background:

Gambling psychopathology is associated with impaired response inhibition.
Neural mechanisms, including GABA_A-mediated neurotransmission in the primary motor cortex (M1), may underlie these impairments.

Purpose of the Study:

To investigate GABA_A and glutamate receptor activity in the M1 of problem gamblers, at-risk gamblers, and controls.
To examine the relationship between M1 neurotransmission markers and response inhibition.

Main Methods:

Used paired-pulse transcranial magnetic stimulation to assess GABA_A and glutamate receptor activity in the left M1.
Administered the stop signal task to measure response inhibition.
Matched participants for alcohol use, substance use, and ADHD symptomology.

Main Results:

Problem gamblers exhibited reduced M1 GABA_A receptor activity compared to controls.
Problem gamblers showed elevated M1 glutamate receptor activity compared to at-risk gamblers and controls.
Poorer response inhibition was correlated with weaker M1 GABA_A receptor activity, despite no group differences in task performance.

Conclusions:

Problem gambling is associated with neurophysiological alterations in M1 GABA_A and glutamate neurotransmission.
These findings suggest a potential neural basis for response inhibition deficits in gambling disorder.