Vipr2, also known as the receptor for vasoactive intestinal peptide (VIP) VPAC2, binds VIP and pituitary adenylate cyclase-activating polypeptide (PACAP) with high affinity. It is involved in regulating various physiological processes, including circadian rhythms, fear cognition, and is associated with the cAMP signaling pathway. Dysregulation of Vipr2 can have significant impacts on brain development, vision, and cancer-related processes [1-5].

In mouse models, Vipr2-knockout (Vipr2-KO) mice show a significant shift towards myopia, suggesting that Vipr2 function is crucial for maintaining normal refractive development. The amplitudes of bipolar cell-derived b-waves in Vipr2-KO mice are larger, indicating compromised bipolar cell function related to changes in signal transduction [1]. Overexpression of Vipr2 in mice leads to microencephaly, a reduction in hippocampus grey matter volume, and an increase in whole-brain white matter volume, along with sex-specific behavioral changes like impaired prepulse inhibition and contextual fear memory, suggesting its role in brain morphogenesis and schizophrenia-related mechanisms [2].

In conclusion, Vipr2 plays essential roles in multiple biological processes. The study of Vipr2-KO and overexpression mouse models has provided valuable insights into its functions in myopia development and schizophrenia-associated brain development. These findings contribute to understanding the underlying mechanisms of these diseases and potentially developing new therapeutic strategies.