甲状腺激素调节新生大鼠培养海马神经元中的钠离子电流。
Thyroid hormone regulates Na+ currents in cultured hippocampal neurons from postnatal rats.
作者信息
Potthoff O, Dietzel I D
机构信息
Department of Molecular Neurobiochemistry, Ruhr-Universität Bochum, Germany.
出版信息
Proc Biol Sci. 1997 Mar 22;264(1380):367-73. doi: 10.1098/rspb.1997.0053.
Abstract
The causes for mental retardation due to perinatal hypothyroidism are not fully understood. Here we show that the most potent component of thyroid hormone, 3,5,3'-triiodo-L-thyronine (T3), selectively increases the density of voltage-activated Na+ currents in hippocampal neurons from newborn rats. Thus, the well known effects of thyroid hormone on energy expenditure and Na+/K+ ATPase activity could to some extent result from the enhanced Na+ influx through voltage-activated Na+ channels. In addition, a down-regulation of the Na+ current density in neurons could contribute to some of the neurological symptoms accompanying hypothyroidism, including slowing of mentation, of neuronal conduction velocities, the alpha rhythm of the electroencephalogram, and increased latencies of evoked potentials and reflexes.
摘要
围产期甲状腺功能减退所致智力发育迟缓的原因尚未完全明确。在此我们发现，甲状腺激素最有效的成分3,5,3'-三碘-L-甲状腺原氨酸（T3）可选择性增加新生大鼠海马神经元中电压门控性Na⁺电流的密度。因此，甲状腺激素对能量消耗及Na⁺/K⁺ATP酶活性的已知作用，在一定程度上可能是由于通过电压门控性Na⁺通道的Na⁺内流增强所致。此外，神经元中Na⁺电流密度的下调可能导致甲状腺功能减退伴随的一些神经症状，包括思维迟缓、神经元传导速度减慢、脑电图α节律减慢以及诱发电位和反射潜伏期延长。
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