Inhibitory spillover: intentional motor inhibition produces incidental limbic inhibition via right inferior frontal cortex

Abstract

Neurocognitive studies have observed rIFC involvement in motor, cognitive, and affective inhibition, suggesting that rIFC is a common inhibitory mechanism across psychological domains. If true, intentional inhibition in one domain may have unintended inhibitory effects ("spillover") in other domains. The present study used an emotional go/no-go task that produces responses in both motor and affective domains, but induces intentional inhibition in only the motor domain. Data support the hypothesis that intentional inhibition in the motor domain, via rIFC, produces inhibitory spillover in the affective domain. Specifically, we observed increased rIFC along with reduced amygdala activity when participants intentionally inhibited motor responses during the presentation of negatively-valenced stimuli, and greater inverse connectivity between these regions during motor inhibition in a PPI analysis. Given the absence of intentional affect regulation, these results suggest that intentional inhibition of a motor response dampens the amygdala activation coincident with affective stimuli to the extent that rIFC activation is higher.

Figure 1

Right inferior frontal cortex (x=40, y=16, z=−18) activation observed during no-go⁻ > go⁻. This region was used as a seed to identify target regions more negatively associated with rIFC during no-go⁻ than go⁻.

Figure 2

Parameter estimates for amygdala (x=−18, y=−4, z=−28) in no-go⁻, go⁻, no-go⁺, and go⁺. There was a significant reduction during no-go⁻ trials (t = −5.12, p < .001) trials, and significant increases during go⁻ and go⁺ trials (ts = 4.55, 5.07, respectively, both ps < .001). There was significantly greater activity during go⁻ than no-go⁻ (t = 6.57, p < .001). Error bars depict 95% confidence interval.

Figure 3

Regions with greater inverse association with right inferior frontal cortex (x=40, y=16, z=−18) during no-go⁻ than baseline include amygdala (x=−26, y=−6, z=−22; x=22, y=−10, z=−22) and anterior insula (x=42, y=18, z=−6).

Figure 4

An example of the inverse functional connectivity between right inferior frontal cortex (x=40, y=16, z=−18) and left amygdala (x=−26, y=−6, z=−22) for a typical subject. Here, the trial-by-trial correlation between rIFC and amygdala was −0.68 during no-go⁻ trials and was 0.07 during go⁻ trials. The psychophysiological analysis (PPI) is a group-level test of the difference of these betas between no-go⁻ and go⁻ trials.