Center for Brain Science, Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts, USA.
Nat Neurosci. 2011 Jul 31;14(9):1189-94. doi: 10.1038/nn.2882.
Neural circuits are shaped by experience during periods of heightened brain plasticity in early postnatal life. Exposure to acoustic features produces age-dependent changes through largely unresolved cellular mechanisms and sites of origin. We isolated the refinement of auditory thalamocortical connectivity by in vivo recordings and day-by-day voltage-sensitive dye imaging in an acute brain slice preparation. Passive tone-rearing modified response strength and topography in mouse primary auditory cortex (A1) during a brief, 3-d window, but did not alter tonotopic maps in the thalamus. Gene-targeted deletion of a forebrain-specific cell-adhesion molecule (Icam5) accelerated plasticity in this critical period. Consistent with its normal role of slowing spinogenesis, loss of Icam5 induced precocious stubby spine maturation on pyramidal cell dendrites in neocortical layer 4 (L4), identifying a primary locus of change for the tonotopic plasticity. The evolving postnatal connectivity between thalamus and cortex in the days following hearing onset may therefore determine a critical period for auditory processing.
神经回路是在出生后早期大脑可塑性增强期间通过经验形成的。通过尚未完全阐明的细胞机制和起源部位，对声音特征的暴露会产生与年龄相关的变化。我们通过在急性脑切片制备中进行体内记录和每日电压敏感染料成像，分离了听觉丘脑皮质连接的细化。在短暂的 3 天窗口期间，被动音调饲养会改变小鼠初级听觉皮层（A1）中的反应强度和拓扑结构，但不会改变丘脑中的音位图谱。前脑特异性细胞黏附分子（Icam5）的基因靶向缺失加速了这一关键时期的可塑性。与其正常的减缓螺旋生成的作用一致，Icam5 的缺失导致新皮层第 4 层（L4）上锥体神经元树突上的短粗棘突提前成熟，确定了音位可塑性的主要变化部位。因此，听觉起始后几天内丘脑和皮层之间的发育中的产后连接可能决定了听觉处理的关键时期。
