The CNR1 gene (Cannabinoid Receptor 1) encodes the CB1 receptor, a highly conserved G protein-coupled receptor (GPCR) that serves as the primary molecular target for endocannabinoids like anandamide and exogenous cannabinoids like THC. It is most abundantly expressed in the central nervous system, particularly in the cerebral cortex, hippocampus, basal ganglia, and cerebellum, but is also present in peripheral tissues such as the liver, adipose tissue, and gastrointestinal tract ^[1]. Functionally, CB1 receptors primarily reside on presynaptic terminals where they regulate neurotransmitter release—typically inhibiting the release of GABA or glutamate—to modulate pain, appetite, memory, and emotional processing ^[2]. Dysregulation of CNR1 expression or CB1 signaling is strongly associated with a variety of diseases, including obesity, metabolic syndrome, chronic pain, and neuropsychiatric disorders, such as anxiety, depression, and schizophrenia ^[3-4].

The huCNR1 mouse is a humanized model constructed by using gene-editing technology to replace the sequence from the ATG start codon to the TGA stop codon in the endogenous mouse Cnr1 gene with the sequence from the ATG start codon to the TGA stop codon in the human CNR1 gene. This model can be used for research related to obesity, metabolic syndrome, chronic pain, and neuropsychiatric diseases, such as anxiety, depression, and schizophrenia, as well as for the development of CNR1-targeted drugs.