Hensch T K, Fagiolini M, Mataga N, Stryker M P, Baekkeskov S, Kash S F
Laboratory for Neuronal Circuit Development, Brain Science Institute RIKEN, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan.
Science. 1998 Nov 20;282(5393):1504-8. doi: 10.1126/science.282.5393.1504.
Sensory experience in early life shapes the mammalian brain. An impairment in the activity-dependent refinement of functional connections within developing visual cortex was identified here in a mouse model. Gene-targeted disruption of one isoform of glutamic acid decarboxylase prevented the competitive loss of responsiveness to an eye briefly deprived of vision, without affecting cooperative mechanisms of synapse modification in vitro. Selective, use-dependent enhancement of fast intracortical inhibitory transmission with benzodiazepines restored plasticity in vivo, rescuing the genetic defect. Specific networks of inhibitory interneurons intrinsic to visual cortex may detect perturbations in sensory input to drive experience-dependent plasticity during development.
早期生活中的感觉体验塑造了哺乳动物的大脑。在此,我们在一个小鼠模型中发现了发育中的视觉皮层内功能连接的活动依赖性精细化受损。谷氨酸脱羧酶一种同工型的基因靶向破坏阻止了对短暂剥夺视力的眼睛反应性的竞争性丧失,而不影响体外突触修饰的协同机制。用苯二氮䓬类药物选择性地、依赖使用增强快速皮质内抑制性传递可恢复体内可塑性,挽救遗传缺陷。视觉皮层固有的抑制性中间神经元的特定网络可能检测感觉输入中的扰动,以驱动发育过程中依赖经验的可塑性。