Selective Suppression of Plasticity in Amygdala Inputs from Temporal Association Cortex by the External Capsule
Selective Suppression of Plasticity in Amygdala Inputs from Temporal Association Cortex by the External Capsule
复制标题
外囊选择性抑制来自颞联合皮层的杏仁核输入的可塑性
作者：
Alexei Morozov;Daniel C. Sukato;Wataru Ito
外囊（EC）中的GABA能神经元在外侧杏仁核（LA）中提供前馈抑制，但EC如何影响来自特定皮质区域的输入的突触传递和可塑性仍然未知;这是因为来自不同皮质区域的轴突纤维在杏仁核中混合，并且不能使用常规电刺激选择性地激活。在这里，我们实现了选择性激活的纤维从颞叶联合皮层（TeA）或前扣带皮层（ACC）通过使用通道视紫红质-2。通过切断EC和LA之间的连接或通过阻断GABAA受体介导的传递来实现贯穿EC的TeA-LA通路中的长时程增强（LTP）。相反，ACC-LA途径中的LTP绕过EC，是GABAA受体非依赖性的。EC横断改变了TeA-LA通路中抑制和兴奋反应之间的平衡，但对ACC-LA通路没有影响。因此，EC提供杏仁核可塑性的通路特异性抑制。
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.