Npy2r-flox Mouse

Npy2r, the Neuropeptide Y receptor Y2, is a key receptor involved in various physiological and psychological processes. It participates in pathways related to the regulation of feeding, anxiety, and pain transmission, among others. Genetic models, such as gene knockout (KO) models, are valuable for studying its functions [1,2,3,5].

In a KO study of Japanese medaka fish, deletion of npy2r increased food intake, with up-regulation of appetite-stimulating genes (agrp, npy) and down-regulation of anorexia factors (cck, pomc). The KO medaka also showed reduced anxiety-like behavior [3]. In mice, lack of Npy2r on proopiomelanocortin (POMC) neurons led to reduced food intake and fat mass, indicating its role in feeding regulation under positive energy balance [2]. Ablating NPY2R-expressing vagal sensory neurons specifically abolished the Bezold-Jarisch reflex, which recapitulates characteristics of human syncope [4]. Pharmacological inhibition of Y2R in mice led to spontaneous pain behavior and mechanical hypersensitivity, highlighting its role in pain transmission gating [5].

In conclusion, Npy2r plays essential roles in regulating feeding, anxiety, pain, and cardiac reflexes. The KO and related models have significantly contributed to understanding its functions in these areas, providing insights into potential therapeutic targets for diseases related to these biological processes.