Reactivated thalamocortical plasticity alters neural activity in sensory-motor cortex during post-critical period

被引:0
作者
Jie, Hyesoo [1 ]
Petrus, Emily [2 ]
Pothayee, Nikorn [1 ]
Koretsky, Alan P. [1 ]
机构
[1] Natl Inst Neurol Disorders & Stroke, NIH, Lab Funct & Mol Imaging, Bethesda, MD 20892 USA
[2] Uniformed Serv Univ Hlth Sci, Dept Anat Physiol & Genet, Bethesda, MD 20814 USA
基金
美国国家卫生研究院;
关键词
Post-critical period neuroplasticity; Thalamocortical input; Homeostatic plasticity; Propagation of neural activity; Whisker primary somatosensory cortex; Whisker primary motor cortex; Whisker secondary somatosensory cortex; RAT BARREL CORTEX; SOMATOSENSORY CORTEX; NEURONAL CIRCUITS; SYNCHRONIZATION; BRAIN; CONNECTIVITY; MODULATION; INDUCTION; DYNAMICS;
D O I
10.1016/j.pneurobio.2025.102735
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neuroplasticity in sensory brain areas supports adaptation after nerve injury and fundamentally impacts sensation and movement. However, limited neuroplasticity in somatosensory areas due to the early critical period makes determining the role of thalamocortical (TC) inputs in sensorimotor signal processing challenging. Here, we demonstrated that reactivation of TC neuroplasticity was associated with an increase in the number of neurons in layer IV (L4) of the whisker primary somatosensory cortex (wS1) with a stable excitation-inhibition ratio. Highly synchronized neural activity in L4 propagated throughout the wS1 column and to the downstream areas, including whisker secondary somatosensory, primary motor cortices, and contralateral wS1. These results provide crucial evidence that TC inputs can alter the neural activity of sensory-motor pathways even after the critical period. Altogether, these enormous changes in sensorimotor circuit activity are important for adaptation following an injury such as limb loss, stroke, or other forms of neural injury.
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页数:11
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