Equipping the Equippers: The Pedagogical and Programmatic Implications of The Christians' Callings in the World Project

When five theological schools realized (a) their graduates affirmed vocation as central to their theology and practice, yet (b) the parishioners of their graduates nevertheless did not feel called, they knew they had to do something. For six years, faculty teams from these schools conducted a variety of experiments in pedagogy, curriculum reform, and program development in order to train their graduates to equip all of God's people to claim and live their vocational identity in the world. This article introduces the identified challenge and necessary theological and pedagogical shift and then describes five of those experiments in greater detail.     

Microstimulation reveals opposing influences of prelimbic and infralimbic cortex on the expression of conditioned fear

Recent studies using lesion, infusion, and unit-recording techniques suggest that the infralimbic (IL) subregion of medial prefrontal cortex (mPFC) is necessary for the inhibition of conditioned fear following extinction. Brief microstimulation of IL paired with conditioned tones, designed to mimic neuronal tone responses, reduces the expression of conditioned fear to the tone. In the present study we used microstimulation to investigate the role of additional mPFC subregions: the prelimbic (PL), dorsal anterior cingulate (ACd), and medial precentral (PrCm) cortices in the expression and extinction of conditioned fear. These are tone-responsive areas that have been implicated in both acquisition and extinction of conditioned fear. In contrast to IL, microstimulation of PL increased the expression of conditioned fear and prevented extinction. Microstimulation of ACd and PrCm had no effect. Under low-footshock conditions (to avoid ceiling levels of freezing), microstimulation of PL and IL had opposite effects, respectively increasing and decreasing freezing to the conditioned tone. We suggest that PL excites amygdala output and IL inhibits amygdala output, providing a mechanism for bidirectional modulation of fear expression.