In the realm of memory, environmental lighting exerts significant influence, impacting various cognitive processes such as fear and object memory. Within this context, our laboratory has previously conducted research demonstrating that brief exposure to light adversely affects social recognition memory (SRM) in mice. Specifically, we found that light exposure hampers the activity of oxytocin neurons located in the supraoptic nucleus (SON) through a pathway involving M1 SON-projecting intrinsically photosensitive retinal ganglion cells (ipRGCs) and GABAergic neurons situated in the perinuclear zone of the SON (pSON). Optogenetic activation of SON oxytocin neurons using channelrhodopsin is sufficient to enhance SRM performance, even under light conditions. To deepen our understanding of how input from RGCs modulates the activity and neuropeptide release of SON magnocellular neurosecretory cells (MNCs), we employed two-photon microscopy to conduct calcium imaging experiments on acute brain slices. Our results confirmed that the optogenetic activation of ipRGC terminals within the SON modulates the neural activity and neuropeptide release of MNCs. This discovery illuminates a specialized neural circuitry through which luminance impacts the functionality of the oxytocin system, utilizing a non-canonical, non-image-forming visual pathway.