Npffr1-flox Mouse

Npffr1, also named GPR147, is the receptor for gonadotropin-inhibitory hormone (GnIH) and can bind neuropeptide FF (NPFF) as well. It is a seven-transmembrane G protein-coupled receptor that inhibits cAMP production. Npffr1 is involved in multiple physiological processes, including the regulation of gonadotropin secretion, nociception, and reproductive function, and is part of the RF-amide peptide system [1,4,5].

In a male mouse model of acute fentanyl-induced analgesia and secondary hyperalgesia, npffr1-/-mice showed a marked reversal of fentanyl-induced hyperalgesia, while the blockade of spinal Npffr1 did not enhance fentanyl-induced analgesia as effectively as the blockade of spinal NPFFR2. This indicates that supraspinal Npffr1 plays a role in modulating fentanyl-induced hyperalgesia [2]. In female rats, the unselective Npffr1 antagonist RF9 and the selective antagonist GJ14 affected the PRL secretion induced by Kp and RFRP-3. GJ14 also blunted the estradiol-induced PRL surge, suggesting that Npffr1 is involved in the control of PRL secretion [3].

In conclusion, Npffr1 is essential in regulating gonadotropin and prolactin secretion, as well as modulating opioid-induced hyperalgesia. Gene knockout mouse models have been valuable in revealing its role in these physiological and pain-related processes, providing insights into potential therapeutic targets for conditions related to abnormal hormone regulation and pain management.