Audiogenic seizure susceptibility in thyroid hormone receptor beta-deficient mice.
Audiogenic seizure susceptibility in thyroid hormone receptor beta-deficient mice.
复制标题
甲状腺激素受体β缺陷小鼠的听源性癫痫易感性。
DOI：
10.1097/00001756-200108080-00015
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发表时间：
2001
期刊：
影响因子：
1.7
通讯作者：
Forrest,D
中科院分区：
文献类型：
--
作者：
Ng,L;Pedraza,PE;Faris,JS;Vennström,B;Curran,T;MorrealedeEscobar,G;Forrest,D
由于早发性甲状腺功能减退症在啮齿类动物中产生听源性癫痫易感性（AGS），因此研究了TRα1和TRβ甲状腺激素受体在AGS中的作用。AGS发生在缺乏特异性TRβ（Thrb tm 1/tm 1）的小鼠中，并以早期发作和持续性为特征，因此与AGS受年龄限制的小鼠品系不同。Thrb tm 1/tm 1小鼠无论是在129/Sv× C57 BL/6 J混合背景下还是在同源C57 BL/6 J背景下均显示AGS。27%的野生型小鼠的混合和0%的同源背景表现出AGS。Thrb tm 1/tm 1小鼠不能下调对持续声刺激的反应可能存在于大脑或听觉系统本身，因为Thrb tm 1/tm 1小鼠也显示听觉缺陷。AGS表型鉴定了TRβ的新神经作用。
As early-onset hypothyroidism produces audiogenic seizure susceptibility (AGS) in rodents, the role of TRα1 and TRβ thyroid hormone receptors in AGS was investigated. AGS occurs in mice lacking specifically TRβ (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× 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 TRβ.