Foote Maxwell K, Huffman William C, Santos Erin N, Lee Philip R, Jarnik Michal, Li Wei, Bonifacino Juan S, Fields R Douglas
Section on Nervous System Plasticity and Development, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.
Retinal Neurophysiology Section, National Eye Institute, National Institutes of Health, Bethesda, MD 20892.
bioRxiv. 2025 Sep 7:2025.09.02.673699. doi: 10.1101/2025.09.02.673699.
Classic experiments showing that monocular visual disruption alters synaptic connections to binocular neurons in the brain established the fundamental concept of synaptic plasticity through coincident spike time arrival. However, if the speed of impulse transmission from the eye is altered by visual deprivation, spike time arrival at binocular neurons would be affected, thereby inducing synaptic plasticity. This possibility is tested here in adult mice by monocular eyelid suture and action potential inhibition in retinal axons. The results show that spike time arrival in visual cortex is altered by monocular visual disruption in association with morphological changes in myelin (nodes of Ranvier) on axons in optic nerve and optic tract. This non-synaptic mechanism of ocular dominance plasticity, mediated by myelin-forming cells, supplements and may drive synaptic plasticity.
经典实验表明，单眼视觉干扰会改变大脑中与双眼神经元的突触连接，通过同步的尖峰时间到达确立了突触可塑性的基本概念。然而，如果视觉剥夺改变了从眼睛传来的冲动传递速度，那么到达双眼神经元的尖峰时间将会受到影响，从而诱导突触可塑性。本文通过成年小鼠的单眼睑缝合以及视网膜轴突动作电位抑制对此可能性进行了测试。结果表明，单眼视觉干扰会改变视觉皮层中尖峰时间的到达，这与视神经和视束轴突上髓鞘（郎飞结）的形态变化有关。这种由形成髓鞘的细胞介导的眼优势可塑性的非突触机制补充并可能驱动突触可塑性。
