Modulating Emotional Experience Using Electrical Stimulation of the Medial-Prefrontal Cortex: A Preliminary tDCS-fMRI Study

Abstract

Objectives: Implicit regulation of emotions involves medial-prefrontal cortex (mPFC) regions exerting regulatory control over limbic structures. Diminished regulation relates to aberrant mPFC functionality and psychopathology. Establishing means of modulating mPFC functionality could benefit research on emotion and its dysregulation. Here, we tested the capacity of transcranial direct current stimulation (tDCS) targeting mPFC to modulate subjective emotional states by facilitating implicit emotion regulation.

Materials and methods: Stimulation was applied concurrently with functional magnetic resonance imaging to validate its neurobehavioral effect. Sixteen participants were each scanned twice, counterbalancing active and sham tDCS application, while undergoing negative mood induction (clips featuring negative vs. neutral contents). Effects of stimulation on emotional experience were assessed using subjective and neural measures.

Results: Subjectively, active stimulation led to significant reduction in reported intensity of experienced emotions to negatively valenced (p = 0.005) clips but not to neutral clips (p > 0.99). Active stimulation further mitigated a rise in stress levels from pre- to post-induction (sham: p = 0.004; active: p = 0.15). Neurally, stimulation increased activation in mPFC regions associated with implicit emotion regulation (ventromedial-prefrontal cortex; subgenual anterior-cingulate cortex, sgACC), and in ventral striatum, a core limbic structure (all ps < 0.05). Stimulation also altered functional connectivity (assessed using whole-brain psycho-physiological interaction) between these regions, and with additional limbic regions. Stimulation-induced sgACC activation correlated with reported emotion intensity and depressive symptoms (rs > 0.64, ps < 0.018), suggesting individual differences in stimulation responsivity.

Conclusions: Results of this study indicate the potential capacity of tDCS to facilitate brain activation in mPFC regions underlying implicit regulation of emotion and accordingly modulate subjective emotional experiences.

Keywords: emotion regulation; fMRI; medial-prefrontal cortex; stimulation; tDCS.

Figure 1. Trial structure, electrode alignment, and session structure

(A) Trial structure in the emotion induction task, which included negative-valence and neutral clips, each followed by a ranking of intensity of emotion elicited by the preceding clip. (B) Electrode alignment during the session: anode electrode in the front, return electrode in the back. (C) Session structure, in terms of current intensity applied (mA, in red), time (minutes), and task (squares and circles). Note: S1 to S4 refer to stress assessments; mA = milliampere.

Figure 2. Effects of stimulation on subjective measures

(A) Mean ratings of experienced emotional intensity in response to presented clips, as a function of clip valence (neutral vs emotional) and stimulation condition (sham vs active). (B) Mean reported stress levels as a function of time (pre- vs post-emotion induction task) and stimulation condition (sham vs active). Note: ** p<0.01. Error bars signify SEM.

Figure 3. Effects of stimulation on brain activation

(A) Sensitivity to stimulation. Slice views of the results obtained from a whole-brain analysis contrasting active minus sham stimulation across all presented clips (p<0.01, FDR-corrected, min cluster size k=50 voxels; n=13). (B) ROI analysis for emotion-specific effects of stimulation, for the hypothesized ROIs in which a significant Stimulation x Valence interaction was observed. Post-hoc analyses revealed that in the vmPFC, sgACC and VS, active stimulation (relative to sham) significantly increased activity during emotional clips, but not during neutral clips. Note: * p<0.05, ** p<0.01. vmPFC = ventromedial prefrontal cortex, sgACC = subgenual anterior cingulate cortex, dmPFC = dorsomedial prefrontal cortex, VS = ventral striatum. Error bars signify SEM.