Inhibitory threshold for critical-period activation in primary visual cortex
Inhibitory threshold for critical-period activation in primary visual cortex
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DOI：
10.1038/35004582
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发表时间：
2000-03-09
期刊：
影响因子：
64.8
通讯作者：
Hensch, TK
中科院分区：
文献类型：
--
作者：
Fagiolini, M;Hensch, TK
在出生后发育期间(1-10)，跨越几个系统的神经元回路对感觉输入显示出显著的可塑性(1-10)。依赖经验的改进通常限于早期生命中明确定义的关键时期，但这些关键时期是如何建立的，目前大多尚不清楚。一个有代表性的例子是大脑皮层对失明眼睛的反应性丧失(2-6)。在这里，我们表明，在达到抑制阈值之前，整个生命都保持着可塑性的潜力。在所有年龄段缺乏GABA(γ-氨基丁酸)合成酶(GAD65)异构体的小鼠中，以及在自然临界期开始之前的未成熟野生型动物中，苯二氮卓类药物选择性地减少延长的放电表型，以揭示可塑性。在生命早期增强GABA介导的传递使突变动物成年后对单眼剥夺不敏感，类似于正常的野生型小鼠。突触前的短期动力学反映了GAD65基因敲除小鼠在慢性安定治疗后的突触重组。因此，视觉皮质内的抑制阈值水平可能会在一生中触发一次依赖经验的电路巩固关键时期，否则可能处于休眠状态。
Neuronal circuits across several systems display remarkable plasticity to sensory input during postnatal development(1-10) Experience-dependent refinements are often restricted to well-defined critical periods in early life, but how these are established remains mostly unknown. A representative example is the loss of responsiveness in neocortex to an eye deprived of vision(2-6). Here we show that the potential for plasticity is retained throughout life until an inhibitory threshold is attained. In mice of all ages lacking an isoform of GABA (gamma-aminobutyric acid) synthetic enzyme (GAD65), as well as in immature wild-type animals before the onset of their natural critical period, benzodiazepines selectively reduced a prolonged discharge phenotype to unmask plasticity. Enhancing GABA-mediated transmission early in life rendered mutant animals insensitive to monocular deprivation as adults, similar to normal wild-type mice. Short-term presynaptic dynamics reflected a synaptic reorganization in GAD65 knockout mice after chronic diazepam treatment. A threshold level of inhibition within the visual cortex may thus trigger, once in life, an experience-dependent critical period for circuit consolidation, which may otherwise lie dormant.