Slitrk1, or SLIT and NTRK-like 1, is a gene encoding a neuronal transmembrane protein. It has abilities in controlling neurite development and synaptic formation, and is involved in regulating noradrenergic and serotonergic systems [2]. It may also participate in pathways related to the development of synapses and is of great biological importance in the context of neuropsychiatric disorders [3]. Genetic models, such as knockout mice, have been crucial in studying its functions.

Slitrk1-KO newborns show abnormal vocalizations, excessive noradrenergic neurites, and reduced Semaphorin3A expression in the prefrontal cortex [1]. Slitrk1-deficient mice display elevated anxiety-like behavior, increased noradrenaline levels, and abnormal serotonergic varicosity size [2,6]. In adult mice, striatal Slitrk1-KD (knock-down) leads to TS-like tic behaviors, impaired prepulse inhibition, and changes in dopaminergic transmission [4]. Also, in a chronic neuropathic pain mouse model, decreased SLITRK1 in the amygdala is associated with anxio-depressive behaviors [5].

In conclusion, Slitrk1 plays a vital role in the development and regulation of neural systems, especially those related to noradrenergic, serotonergic, and dopaminergic transmissions. The study of Slitrk1 through KO and KD mouse models has significantly contributed to understanding the pathophysiology of neuropsychiatric disorders such as Tourette's syndrome, obsessive-compulsive disorder, and anxiety-related disorders [1,2,4,6].