Influences of un-modulated acoustic inputs on functional maturation and critical-period plasticity of the primary auditory cortex.
Influences of un-modulated acoustic inputs on functional maturation and critical-period plasticity of the primary auditory cortex.
复制标题
未调制的声输入对初级听觉皮层功能成熟和关键期可塑性的影响。
DOI：
10.1016/j.neuroscience.2008.01.026
复制
发表时间：
2008
期刊：
影响因子：
3.3
通讯作者：
Merzenich,MM
中科院分区：
文献类型：
--
作者：
Zhou,X;Nagarajan,N;Mossop,BJ;Merzenich,MM
在哺乳动物出生后发育的“关键时期”，感官体验有助于哺乳动物听觉系统信号处理能力的发展和专业化。早期的研究已经表明，在出生后时期被动暴露于音调刺激会引起初级听觉皮层（A1）内这些刺激的表征的大规模扩展[Zhang LI，Bao S，梅尔泽尼希MM（2001）Persistent and specific influences of early acoustic environments on primary auditory cortex. Nat Neurosci 4：1123-1130]。在这里，我们表明，暴露大鼠幼崽通过正常的关键时期的时代和超越连续的，未调制的，中等水平的音调诱导没有这样的代表性失真，实际上破坏了整个区域A1的频率响应的选择性和tonotopicity的正常发展。与在正常环境中饲养的大鼠相比，大脑皮层对持续暴露的声音频率有选择性反应的区域实际上减少了。通过简单地调节音调刺激，可以在超过正常临界期结束的时间内诱导出强的临界期可塑性特征。因此，连续音暴露，如连续噪声暴露[Chang EF，梅尔泽尼希MM（2003）环境噪声阻碍听觉皮层发育。Science 300：498-502]，无效地诱导关键期可塑性，并且无限期地阻止正常短暂的关键期窗口的关闭。这些发现再次证明了时间结构输入的关键作用，诱导渐进的皮层成熟的变化，导致关闭的关键期窗口。
Sensory experiences contribute to the development and specialization of signal processing capacities in the mammalian auditory system during a “critical period” of postnatal development. Earlier studies have shown that passive exposure to tonal stimuli during this postnatal epoch induces a large-scale expansion of the representations of those stimuli within the primary auditory cortex (A1) [Zhang LI, Bao S, Merzenich MM (2001) Persistent and specific influences of early acoustic environments on primary auditory cortex. Nat Neurosci 4:1123–1130]. Here, we show that exposing rat pups through the normal critical period epoch and beyond to continuous, un-modulated, moderate-level tones induces no such representational distortion, and in fact disrupts the normal development of frequency response selectivity and tonotopicity all across area A1. The area of cortex responding selectively to continuously exposed sound frequencies was actually reduced, when compared with rats reared in normal environments. Strong exposure-driven plasticity characteristic of the critical period could be induced well beyond the normal end of the critical period, by simply modulating the tonal stimulus. Thus, continuous tone exposure, like continuous noise exposure [Chang EF, Merzenich MM (2003) Environmental noise retards auditory cortical development. Science 300:498–502], ineffectively induces critical period plasticity, and indefinitely blocks the closure of a normally-brief critical period window. These findings again demonstrate the crucial role of temporally structured inputs for inducing the progressive cortical maturational changes that result in the closure of the critical period window.