| First Author | Toriumi K | Year | 2018 |
| Journal | Behav Brain Res | Volume | 339 |
| Pages | 207-214 | PubMed ID | 29203337 |
| Mgi Jnum | J:261161 | Mgi Id | MGI:6120336 |
| Doi | 10.1016/j.bbr.2017.11.040 | Citation | Toriumi K, et al. (2018) Shati/Nat8l knockout mice show behavioral deficits ameliorated by atomoxetine and methylphenidate. Behav Brain Res 339:207-214 |
| abstractText | We previously identified a novel molecule, SHATI/NAT8L, as having an inhibitory effect on methamphetamine dependence. We generated Shati/Nat8l knockout (KO) mice and found that they showed neurochemical changes and behavioral abnormalities related to attention deficit/hyperactivity disorder (AD/HD). In this study, we assessed validities of the Shati/Nat8l KO mice as a new animal model for AD/HD through a behavioral pharmacology approach. We conducted a locomotor activity test in a novel environment, a cliff avoidance test, and an object-based attention assay using Shati/Nat8l KO mice at the ages of 4 and 8 weeks. We found that at the ages of both 4 and 8 weeks, Shati/Nat8l KO mice showed hyperactivity in locomotor activity test, shortened jumping latency in cliff avoidance test, and lower recognition index in object-based recognition test. Moreover, we evaluated the effects of atomoxetine (ATX) and methylphenidate (MPH) on the behavioral deficits in Shati/Nat8l KO mice. As the result, almost all behavioral deficits were improved by the treatment of both ATX and MPH. Our findings suggest that Shati/Nat8l KO mice have an impaired neural system similar to AD/HD pathophysiology. Shati/Nat8l KO mice might serve as a novel and a useful animal model for the pathophysiology of AD/HD. |
