Mascha van 't Wout1, Timothy Y Mariano2, Sarah L Garnaat3, Madhavi K Reddy3, Steven A Rasmussen2, Benjamin D Greenberg2. 1. Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Butler Hospital, 345 Blackstone Boulevard, Providence, RI 02906, USA; Center of Excellence for Neurorestoration and Neurotechnology, Providence Veterans Affairs Medical Center, 830 Chalkstone Avenue, Providence, RI 02908, USA. Electronic address: maschavantwout@gmail.com. 2. Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Butler Hospital, 345 Blackstone Boulevard, Providence, RI 02906, USA; Center of Excellence for Neurorestoration and Neurotechnology, Providence Veterans Affairs Medical Center, 830 Chalkstone Avenue, Providence, RI 02908, USA. 3. Department of Psychiatry and Human Behavior, Alpert Medical School of Brown University, Butler Hospital, 345 Blackstone Boulevard, Providence, RI 02906, USA.
Abstract
BACKGROUND: Exposure-based therapy parallels extinction learning of conditioned fear. Prior research points to the ventromedial prefrontal cortex as a potential site for the consolidation of extinction learning and subsequent retention of extinction memory. OBJECTIVE/HYPOTHESIS: The present study aimed to evaluate whether the application of non-invasive transcranial direct current stimulation (tDCS) during extinction learning enhances late extinction and early recall in human participants. METHODS: Forty-four healthy volunteers completed a 2-day Pavlovian fear conditioning, extinction, and recall paradigm while skin conductance activity was continuously measured. Twenty-six participants received 2 mA anodal tDCS over EEG coordinate AF3 during extinction of a first conditioned stimulus. The remaining 18 participants received similar tDCS during extinction of a second conditioned stimulus. Sham stimulation was applied for the balance of extinction trials in both groups. Normalized skin conductance changes were analyzed using linear mixed models to evaluate effects of tDCS over late extinction and early recall trials. RESULTS: We observed a significant interaction between timing of tDCS during extinction blocks and changes in skin conductance reactivity over late extinction trials. These data indicate that tDCS was associated with accelerated late extinction learning of a second conditioned stimulus after tDCS was combined with extinction learning of a previous conditioned stimulus. No significant effects of tDCS timing were observed on early extinction recall. CONCLUSIONS: Results could be explained by an anxiolytic aftereffect of tDCS and extend previous studies on tDCS-induced modulation of fear and threat related learning processes. These findings support further exploration of the clinical use of tDCS.
BACKGROUND: Exposure-based therapy parallels extinction learning of conditioned fear. Prior research points to the ventromedial prefrontal cortex as a potential site for the consolidation of extinction learning and subsequent retention of extinction memory. OBJECTIVE/HYPOTHESIS: The present study aimed to evaluate whether the application of non-invasive transcranial direct current stimulation (tDCS) during extinction learning enhances late extinction and early recall in humanparticipants. METHODS: Forty-four healthy volunteers completed a 2-day Pavlovian fear conditioning, extinction, and recall paradigm while skin conductance activity was continuously measured. Twenty-six participants received 2 mA anodal tDCS over EEG coordinate AF3 during extinction of a first conditioned stimulus. The remaining 18 participants received similar tDCS during extinction of a second conditioned stimulus. Sham stimulation was applied for the balance of extinction trials in both groups. Normalized skin conductance changes were analyzed using linear mixed models to evaluate effects of tDCS over late extinction and early recall trials. RESULTS: We observed a significant interaction between timing of tDCS during extinction blocks and changes in skin conductance reactivity over late extinction trials. These data indicate that tDCS was associated with accelerated late extinction learning of a second conditioned stimulus after tDCS was combined with extinction learning of a previous conditioned stimulus. No significant effects of tDCS timing were observed on early extinction recall. CONCLUSIONS: Results could be explained by an anxiolytic aftereffect of tDCS and extend previous studies on tDCS-induced modulation of fear and threat related learning processes. These findings support further exploration of the clinical use of tDCS.
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