Electroacupuncture activation of the CaMKII/CREB pathway improves dLGN synaptic plasticity in monocular deprivation amblyopic rats.

OBJECTIVE

This study aimed to investigate the therapeutic potential of electroacupuncture(EA) for amblyopia, a common childhood visual disorder caused by early abnormalities such as monocular deprivation(MD). We examined the role of the calcium/calmodulin-dependent protein kinase II/cAMP response element-binding protein(CaMKII/CREB) pathway and enhanced synaptic plasticity in visual function improvement following EA.

METHODS

An amblyopia model was established using 14-day-old rats by inducing MD during a critical developmental period. MD rats received EA stimulation at the Cuanzhu(BL2) and Fengchi(GB20) acupoints for 14 consecutive days. Visual function was assessed. Structural damage to the retina and dorsal lateral geniculate nucleus(dLGN) was analyzed. CaMKII/CREB pathway and synaptic plasticity proteins(SYN1 and PSD95) activity levels were measured. To confirm CaMKII involvement, the inhibitor KN93 was administered.

RESULTS

EA was associated with significant visual function improvement in rats MD with and reduced structural damage to retinal and dLGN cells. EA activated the CaMKII/CREB signaling pathway and upregulated synaptic plasticity protein(SYN1 and PSD95) expression. The therapeutic effects of EA were markedly attenuated when the CaMKII inhibitor KN93 was co-administered, demonstrating that CaMKII signaling is essential for mediating the benefits of EA.

CONCLUSION

EA effectively treated amblyopia in this model by restoring visual function and protecting neural structures by activating the CaMKII/CREB signaling pathway, subsequently enhancing synaptic plasticity. These findings provide a strong theoretical foundation for the clinical application of EA in the treatment of amblyopia.