Audiogenic seizure susceptibility in thyroid hormone receptor β-deficient mice

被引:22
作者
Ng, L
Pedraza, PE
Faris, JS
Vennström, B
Curran, T
de Escobar, GM
Forrest, D
机构
[1] CSIC, Inst Invest Biomed, E-28029 Madrid, Spain
[2] CUNY Mt Sinai Sch Med, Dept Human Genet, New York, NY 10029 USA
[3] Univ Autonoma Madrid, Madrid 28029, Spain
[4] Karolinska Inst, CMB, S-17177 Stockholm, Sweden
[5] St Jude Childrens Res Hosp, Dept Dev Neurobiol, Memphis, TN 38105 USA
关键词
audiogenic seizures; auditory system; thyroid hormone receptor;
D O I
10.1097/00001756-200108080-00015
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
As early-onset hypothyroidism produces audiogenic seizure susceptibility (AGS) in rodents, the role of TR alpha1 and TR beta thyroid hormone receptors in AGS was investigated. AGS occurs in mice lacking specifically TR beta (Thrb(tm1/tm1)) and is marked by early onset and persistence, thereby differing from mouse strains where AGS is age-restricted. Thrb(tm1/tm1) mice display AGS whether on a mixed 129/Sv x C57BL/6J or congenic C57BL/6J background. 27% of wild-type mice on the mixed and 0% on the congenic background exhibited AGS. The inability of Thrb(tm1/tm1) mice to downregulate the response to sustained acoustic stimulation may reside in the brain or in the auditory system itself as Thrb(tm1/tm1) mice also display auditory deficits. The AGS phenotype identifies a novel neurological role for TR beta. NeuroReport 12:2359-2362 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:2359 / 2362
页数:4
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