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<p>The plasticity of ocular dominance is most prominent during the critical period of visual development, influenced by the balance of excitatory and inhibitory synaptic transmission in the visual cortex. Astrocytes play a crucial role in regulating synaptic plasticity through phagocytosis of synapses. However, the ability of astrocytes to modulate synaptic plasticity after the critical period remains unclear. Oxytocin (OT), a neuropeptide involved in neural circuit formation, has shown potential in enhancing synaptic plasticity. This study explores the role of OT in restoring visual cortical plasticity during and after the critical period of visual development. We performed monocular deprivation (MD) on mice during the critical period and extended the deprivation until adulthood. Visual cortical plasticity was evaluated using pattern visual evoked potentials (PVEPs), immunofluorescence staining, and western blotting. Excitatory synaptic markers (VGLUT1, PSD- 95) and inhibitory synaptic markers (VGAT, Gephyrin) were analyzed. The effects of OT administration, alone or combined with reverse occlusion (RO), on ocular dominance plasticity and astrocyte activity were assessed. During the critical period, MD induced a significant ocular dominance shift with reduced cortical response from the deprived eye, primarily through decreased excitatory synaptic markers (VGLUT1: <i>P</i> &lt; 0.05; PSD- 95: <i>P</i> &lt; 0.05). OT administration further enhanced this shift by reducing GFAP expression and decreasing astrocytic phagocytosis of excitatory synapses. After the critical period, prolonged MD reduced excitatory synaptic marker expression in the visual cortex (<i>P</i> &lt; 0.05), and RO alone did not restore cortical plasticity. However, the combination of OT and RO increased excitatory synaptic marker expression (VGLUT1: <i>P</i> &lt; 0.05; PSD- 95: <i>P</i> &lt; 0.05 and restored ocular dominance plasticity. Our findings demonstrate that OT can modulate astrocyte activity and enhance excitatory synaptic plasticity, facilitating the recovery of visual cortical plasticity both during and after the critical period. These results highlight the potential of OT as a therapeutic intervention for visual impairments caused by disrupted sensory experiences during development.</p>

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The impact of exogenous Oxytocin on visual cortex plasticity across different stages of visual development

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月9日

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  • Yifan Sun,
  • Xiao Wang,
  • Yamin Chen,
  • Zichen Luan,
  • Rui Hao

摘要

The plasticity of ocular dominance is most prominent during the critical period of visual development, influenced by the balance of excitatory and inhibitory synaptic transmission in the visual cortex. Astrocytes play a crucial role in regulating synaptic plasticity through phagocytosis of synapses. However, the ability of astrocytes to modulate synaptic plasticity after the critical period remains unclear. Oxytocin (OT), a neuropeptide involved in neural circuit formation, has shown potential in enhancing synaptic plasticity. This study explores the role of OT in restoring visual cortical plasticity during and after the critical period of visual development. We performed monocular deprivation (MD) on mice during the critical period and extended the deprivation until adulthood. Visual cortical plasticity was evaluated using pattern visual evoked potentials (PVEPs), immunofluorescence staining, and western blotting. Excitatory synaptic markers (VGLUT1, PSD- 95) and inhibitory synaptic markers (VGAT, Gephyrin) were analyzed. The effects of OT administration, alone or combined with reverse occlusion (RO), on ocular dominance plasticity and astrocyte activity were assessed. During the critical period, MD induced a significant ocular dominance shift with reduced cortical response from the deprived eye, primarily through decreased excitatory synaptic markers (VGLUT1: P < 0.05; PSD- 95: P < 0.05). OT administration further enhanced this shift by reducing GFAP expression and decreasing astrocytic phagocytosis of excitatory synapses. After the critical period, prolonged MD reduced excitatory synaptic marker expression in the visual cortex (P < 0.05), and RO alone did not restore cortical plasticity. However, the combination of OT and RO increased excitatory synaptic marker expression (VGLUT1: P < 0.05; PSD- 95: P < 0.05 and restored ocular dominance plasticity. Our findings demonstrate that OT can modulate astrocyte activity and enhance excitatory synaptic plasticity, facilitating the recovery of visual cortical plasticity both during and after the critical period. These results highlight the potential of OT as a therapeutic intervention for visual impairments caused by disrupted sensory experiences during development.