Thyroid hormone regulates Na+ currents in cultured hippocampal neurons from postnatal rats.
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.
Potthoff
O
O
Department of Molecular Neurobiochemistry, Ruhr-Universität Bochum, Germany.
Dietzel
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ID
D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D005071:Evoked Potentials / Q000187:drug effects; D006624:Hippocampus / Q000502:physiology*; D015640:Ion Channel Gating / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D009431:Neural Conduction; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D014284:Triiodothyronine / Q000494:pharmacology*
D015221:Potassium Channels; D015222:Sodium Channels; D014284:Triiodothyronine