Abstract
GABAergic neurons in the external capsule (EC) provide feedforward inhibition in the lateral amygdala (LA), but how EC affects synaptic transmission and plasticity in inputs from specific cortical areas remains unknown; this is because axonal fibers from different cortical areas are intermingled in the amygdala and cannot be activated selectively using conventional electrical stimulation. Here, we achieved selective activation of fibers from the temporal association cortex (TeA) or the anterior cingulate cortex (ACC) by using channelrhodopsin-2. Long-term potentiation (LTP) in the TeA–LA pathway, which runs through EC, was enabled by cutting connections between EC and LA or by blocking GABAA receptor-mediated transmission. In contrast, LTP in the ACC–LA pathway, which bypasses EC, was GABAA receptor independent. The EC transection shifted balance between inhibitory and excitatory responses in the TeA–LA pathway toward excitation, but had no effect on the ACC–LA pathway. Thus, EC provides pathway-specific suppression of amygdala plasticity.
