Fig. 1

Pathophysiology of myopia and mode of action of blind spot stimulation. A Hyperopic defocus significantly alters neuronal signal processing in the retina and reduces dopamine release from amacrine cells (Troilo et al. 2019), resulting in a dopaminergic deficiency that is associated with choroidal thinning. The effects on the sclera are numerous: degradation of collagen, thinning of the sclera, loss of cross-linking resulting in mechanical destabilization. Because of the difference in pressure between the inside and outside of the eye, these factors cause axial elongation of the eye, leading to myopia (Chakraborty et al. 2020; Németh et al. 2021; Troilo et al. 2019). The effect of daylight on the development of axial length is mediated by the neurotransmitter dopamine (Cohen et al. 2012; Muralidharan et al. 2021; Zhang and Deng 2020). Daylight activates the photopigment melanopsin, which is localized in the axons’ membrane of ipRGC. This activation increases the release of dopamine in the retina via an excitatory synaptic contact to dopaminergic amacrine cells. Blue light stimulation of the blind spot is suggested to stimulate melanopsin in the same way as daylight since this site of stimulation offers the possibility of exciting as many melanopsin-containing axons of ipRGC as possible through a relatively small light stimulus. The activation of ipRGC may result in increased dopamine release and inhibition of the pathophysiological signaling cascade of myopia. B The dopamine release from DAC in the retina is influenced by excitatory ( +) and inhibitory (-) signaling pathways from different photoreceptors (Newkirk et al. 2013). The activation of the photopigment melanopsin, located on ipRGC, has a direct monosynaptic (solid line) excitatory effect on DAC. Rods and cones indirectly affect the DAC via interneurons, as indicated by the dashed lines. It is assumed that rods inhibit DAC through two synapses by releasing the inhibitory neurotransmitter glycine. Cones can excite DAC through the ON signaling pathway via glutamate and inhibit DAC through the OFF signaling pathway via gamma-aminobutyric acid (GABA). C Blue light stimulation of the blind spot activates the melanopsin photopigments on the ipRGC. Various studies are described that have investigated the effect on contrast sensitivity (Schilling et al. 2023), retinal activity (Amorim-de-Sousa et al. 2021; Schilling et al. 2022) and the biomarkers choroidal thickness and axial length (Chakraborty et al. 2024; Ellrich et al. 2023; Hoseini-Yazdi et al. 2024). The possible mechanism of action of blind spot stimulation with blue light via melanopsin-containing ipRGC via retinal dopamine release by DAC on the surrogate markers is shown