Tacr3 encodes tachykinin receptor 3 (NK3R), belonging to the tachykinin receptor family within the rhodopsin subfamily of G protein-coupled receptors. It functions by binding to its high-affinity ligand, neurokinin B (NKB), and is involved in various biological processes. In growth and reproduction, it has been well-studied, and also plays roles in the nervous system, participating in physiological and pathological processes like mood disorders, chronic pain, and neurodegenerative diseases [1].

In a mouse model of trigeminal neuralgia, downregulation of Tacr3 in the lateral habenula (LHb) was observed, and rescuing this downregulation by overexpressing Tacr3 in the unilateral LHb reversed anxiety-like behaviors but not allodynia. Bilateral Tacr3 overexpression in the LHb alleviated both allodynia and anxiety-like behaviors, suggesting Tacr3 in the LHb suppresses the hyperexcitability of LHb neurons and plays a protective role [3]. In rats, severe anxiety is linked to dampened TACR3 expression in the ventral hippocampus, and TACR3 expression is sensitive to sex hormones. Inhibition of TACR3 activity affects synaptic activity, spine density, and long-term potentiation (LTP), indicating its role in regulating anxiety-associated synaptic plasticity [2].

In conclusion, Tacr3 is essential in regulating reproduction-related functions and has a significant impact on the nervous system, especially in relation to mood-related behaviors and synaptic plasticity. The study of Tacr3 in mouse models has provided valuable insights into its role in conditions such as trigeminal neuralgia-related mood disorders and anxiety-associated neural changes, which may offer potential therapeutic targets for these diseases.