According to the prefrontal-subcortical model of emotion regulation, the prefrontal cortex (PFC) regulates the limbic system, especially the amygdala, and puts it under control in face of negative stress (Davidson, 2002;Ochsner & Gross, 2005;Ochsner et al., 2012). When the PFC is dysfunctional, the amygdala may become out of control (e.g., overactive), leading to the emergence of affective disorders. Over the past few decades, this neural model, proposed to explain affective disorders, has received abundant empirical support (Dougherty & Rauch, 1997;Drevets, 2001;Karl et al., 2006). For example, some single-photon emission computed tomography (SPECT) and positron emission tomography (PET) studies have reported glucose hypometabolism in the frontal lobes of patients with mood disorders and a relationship between the severity of depression and frontal hypometabolism (