Journal
NEUROREPORT
Volume 12, Issue 11, Pages 2359-2362Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200108080-00015
Keywords
audiogenic seizures; auditory system; thyroid hormone receptor
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Funding
- NCI NIH HHS [P30 CA 84139] Funding Source: Medline
- NIDCD NIH HHS [DC-03441] Funding Source: Medline
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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.
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