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Motor cortex dysfunction in problem gamblers
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DOI：10.1111/adb.12871.png)
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Impairments in response inhibition have been implicated in gambling psychopathology. This behavioral impairment may suggest that the neural mechanisms involved in response inhibition, such as GABA(A)-mediated neurotransmission in the primary motor cortex (M1), are also impaired. The present study obtained paired-pulse transcranial magnetic stimulation markers of GABA(A) and glutamate receptor activity from the left M1 of three groups-problem gamblers (n = 17, 12 males), at-risk gamblers (n = 29, 19 males), and controls (n = 23, six males)-with each group matched for alcohol use, substance use, and attention-deficit hyperactivity disorder (ADHD) symptomology. Response inhibition was measured using the stop signal task. Results showed that problem gamblers had weaker M1 GABA(A) receptor activity relative to controls and elevated M1 glutamate receptor activity relative to at-risk gamblers and controls. Although there were no differences in response inhibition between the groups, poorer response inhibition was correlated with weaker M1 GABA(A) receptor activity. These findings are the first to show that problem gambling is associated with alterations in M1 GABA(A) and glutamate-mediated neurotransmission.
Keyword:
GABA
glutamate
impulsivity
problem gambling
response inhibition
transcranial magnetic stimulation
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