CHRNA7, the gene encoding the α7 neuronal nicotinic acetylcholine receptor, is ubiquitously expressed in the central nervous system and periphery. It is involved in cholinergic neurotransmission, and its function is crucial for normal cognitive processes. The regulation of CHRNA7 is complex, with a partial duplication resulting in the chimeric CHRFAM7A gene that exerts dominant-negative regulation [1].

In animal models, Chrna7 deficient mice have been studied. One study found that they did not show consistent neuropsychiatric and behavioral phenotypes related to those seen in humans, suggesting mouse behavior and EEG recordings may not be sensitive to decreased Chrna7 copy number [2]. Another study showed that Chrna7 knock-out (KO) mice display depression-like behaviors, and splenic nerve denervation can attenuate these behaviors via the spleen-gut-brain axis, indicating the splenic nerve contributes to depression-like phenotypes in these KO mice [3].

In conclusion, CHRNA7 plays a significant role in cholinergic neurotransmission and is associated with multiple disorders such as schizophrenia, bipolar disorder, and Alzheimer's disease. Mouse models, especially Chrna7 KO mice, have provided insights into the gene's role in depression-like behaviors, though their overall utility in mimicking human neuropsychiatric phenotypes remains somewhat limited.