@article{oai:nagasaki-u.repo.nii.ac.jp:00027634,
 author = {Hatayama, Minoru and Katayama, Kei-ichi and Kawahara, Yukie and Matsunaga, Hayato and Takashima, Noriko and Iwayama, Yoshimi and Matsumoto, Yoshifumi and Nishi, Akinori and Yoshikawa, Takeo and Aruga, Jun},
 issue = {1},
 journal = {Communications Biology},
 month = {Sep},
 note = {SLITRK1 is an obsessive-compulsive disorder spectrum-disorders-ssociated gene that encodes a neuronal transmembrane protein. Here we show that SLITRK1 suppresses noradrenergic projections in the neonatal prefrontal cortex, and SLITRK1 functions are impaired by SLITRK1 mutations in patients with schizophrenia (S330A, a revertant of Homo sapiensspecific residue) and bipolar disorder (A444S). Slitrk1-KO newborns exhibit abnormal vocalizations, and their prefrontal cortices show excessive noradrenergic neurites and reduced Semaphorin3A expression, which suppresses noradrenergic neurite outgrowth in vitro. Slitrk1 can bind Dynamin1 and L1 family proteins (Neurofascin and L1CAM), as well as suppress Semaphorin3A-induced endocytosis. Neurofascin-binding kinetics is altered in S330A and A444S mutations. Consistent with the increased obsessive-compulsive disorder prevalence in males in childhood, the prefrontal cortex of male Slitrk1-KO newborns show increased noradrenaline levels, and serotonergic varicosity size. This study further elucidates the role of noradrenaline in controlling the development of the obsessive-compulsive disorder-related neural circuit., Communications Biology, 5 (1), art. no. 935},
 title = {SLITRK1-mediated noradrenergic projection suppression in the neonatal prefrontal cortex},
 volume = {5},
 year = {2022}
}