Chrnb3, encoding the cholinergic receptor nicotinic beta 3 subunit, is a key component of nicotinic acetylcholine receptors (nAChRs). These ligand-gated ion channels are involved in the neurotransmission process, and Chrnb3-containing nAChRs play important roles in the nervous system. The gene is associated with pathways related to nicotine and alcohol dependence, as well as potential implications in diseases like Parkinson's disease and schizophrenia [2,3,4,6]. Genetic models, such as transgenic mice, are valuable tools for studying Chrnb3's function.

A Chrnb3-Cre BAC transgenic mouse line was characterized, where Cre expression was restricted to retinal ganglion cells (RGCs) in the retina and sparsely expressed in the brain, excluding retinorecipient regions. This tool is useful for studying RGC-specific contributions of genes to visual circuit development [1]. Functional studies in mice have shown that the CHRNB3-CHRNA6 gene cluster on chromosome 8, including Chrnb3, is crucial for nicotine dependence. For example, α6 *-nAChRs in the ventral tegmental area (VTA), which may involve Chrnb3, are important in controlling nicotine self-administration [2]. Also, in a Korean population, polymorphisms in Chrnb3 and CHRNA6 were associated with a nicotine dependence endophenotype (drive) using the nicotine dependence syndrome scale (NDSS) subscales [5].

In conclusion, Chrnb3 is significant for its role in nAChR-mediated neurotransmission. The use of Chrnb3-Cre transgenic mouse models has advanced our understanding of its function in visual circuit development. Moreover, research on Chrnb3 in mouse models has provided insights into nicotine dependence, highlighting its importance in understanding the genetic basis of this disorder.