PDF(Pubmed)
Abstract：
Corticofugal projections to evolutionarily ancient, subcortical structures are ubiquitous across mammalian sensory systems. These \'descending\' pathways enable the neocortex to control ascending sensory representations in a predictive or feedback manner, but the underlying cellular mechanisms are poorly understood. Here, we combine optogenetic approaches with in vivo and in vitro patch-clamp electrophysiology to study the projection from mouse auditory cortex to the inferior colliculus (IC), a major descending auditory pathway that controls IC neuron feature selectivity, plasticity, and auditory perceptual learning. Although individual auditory cortico-collicular synapses were generally weak, IC neurons often integrated inputs from multiple corticofugal axons that generated reliable, tonic depolarizations even during prolonged presynaptic activity. Latency measurements in vivo showed that descending signals reach the IC within 30 ms of sound onset, which in IC neurons corresponded to the peak of synaptic depolarizations evoked by short sounds. Activating ascending and descending pathways at latencies expected in vivo caused a NMDA receptor-dependent, supralinear excitatory postsynaptic potential summation, indicating that descending signals can nonlinearly amplify IC neurons\' moment-to-moment acoustic responses. Our results shed light upon the synaptic bases of descending sensory control and imply that heterosynaptic cooperativity contributes to the auditory cortico-collicular pathway\'s role in plasticity and perceptual learning.
摘要：
对进化上古老的皮质预测，皮层下结构在哺乳动物的感觉系统中无处不在.这些“下降”路径使大脑皮层能够以预测或反馈的方式控制上升的感觉表征，但是对潜在的细胞机制知之甚少。这里,我们将光遗传学方法与体内和体外膜片钳电生理学相结合，研究从小鼠听觉皮层到下丘（IC）的投射，控制IC神经元特征选择性的主要下降听觉通路，可塑性,和听觉知觉学习。尽管单个听觉皮质-丘突触通常很弱，IC神经元通常会整合来自多个皮质胶质轴突的输入，这些轴突产生了可靠的，即使在延长的突触前活动期间，也会出现强直去极化。体内的潜伏期测量表明，下降信号在声音开始的30毫秒内到达IC，在IC神经元中，它对应于由短声引起的突触去极化的峰值。在体内预期的潜伏期激活上升和下降途径导致NMDA受体依赖性，超线性兴奋性突触后电位总和，表明下降信号可以非线性地放大IC神经元的瞬间声学响应。我们的结果揭示了感觉控制下降的突触基础，并暗示异质突触协同作用有助于听觉皮质-丘通路在可塑性和知觉学习中的作用。
