| First Author | Siesser WB | Year | 2005 |
| Journal | Psychopharmacology (Berl) | Volume | 181 |
| Issue | 4 | Pages | 653-63 |
| PubMed ID | 15983791 | Mgi Jnum | J:114325 |
| Mgi Id | MGI:3688782 | Doi | 10.1007/s00213-005-0024-5 |
| Citation | Siesser WB, et al. (2005) Hyperactivity, impaired learning on a vigilance task, and a differential response to methylphenidate in the TRbetaPV knock-in mouse. Psychopharmacology (Berl) 181(4):653-63 |
| abstractText | RATIONALE: The thyroid hormones (T3 and T4) play a critical role in brain development, and thyroid abnormalities have been linked to a variety of psychiatric and neuropsychological disorders. Among patients with the rare genetic syndrome resistance to thyroid hormone (RTH), 40-70% meet the diagnostic criteria for attention deficit-hyperactivity disorder (ADHD). RTH is caused by a mutation in the thyroid receptor beta (Thrb) gene that results in reduced binding of T3 to its receptor and elevated concentrations of T3, T4, and thyroid-stimulating hormone. OBJECTIVES: We tested a knock-in (KI) mouse expressing a mutant TRbeta allele (TRbetaPV) for the behavioral features of ADHD and their response to methylphenidate (MPH). METHODS: The locomotor activity of the TRbetaPV KI mice was measured in activity monitors over multiple sessions. Sustained attention and the effects of MPH on attention were assessed using a vigilance task. RESULTS: The TRbetaPV KI mice are hyperactive and have learning deficits on a vigilance task. Doses of MPH that impair the vigilance performance of wild-type mice do not affect the performance of the TRbetaPV KI mice. CONCLUSIONS: The TRbetaPV KI mice provide a tool for studying the underlying neural deficits that contribute to thyroid-related neurological disorders, hyperactivity, and altered responsiveness to MPH. |
