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Molecular Endocrinology, doi:10.1210/me.2009-0132
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Molecular Endocrinology 23 (9): 1494-1504
Copyright © 2009 by The Endocrine Society

Thyroid Hormone (T3)-Induced Up-Regulation of Voltage-Activated Sodium Current in Cultured Postnatal Hippocampal Neurons Requires Secretion of Soluble Factors from Glial Cells

Vanessa Niederkinkhaus, Romy Marx, Gerd Hoffmann and Irmgard D. Dietzel

Department of Molecular Neurobiochemistry (V.N., R.M., G.H., I.D.D.) and International Graduate School of Neuroscience (V.N., I.D.D.), Ruhr-University Bochum, NC7/170, D-44780 Bochum, Germany

Address all correspondence and requests for reprints to: Irmgard D. Dietzel, Department of Molecular Neurobiochemistry, Ruhr-University Bochum, NC7-170, Universitätsstrasse 150, D-44780 Bochum, Germany. E-mail: Irmgard.D.Dietzel-Meyer{at}ruhr-uni-bochum.de.

We have previously shown that treatment with the thyroid hormone T3 increases the voltage-gated Na+current density (Nav-D) in hippocampal neurons from postnatal rats, leading to accelerated action potential upstrokes and increased firing frequencies. Here we show that the Na+ current regulation depends on the presence of glial cells, which secrete a heat-instable soluble factor upon stimulation with T3. The effect of conditioned medium from T3-treated glial cells was mimicked by basic fibroblast growth factor (bFGF), known to be released from cerebellar glial cells after T3 treatment. Neutralization assays of astrocyte-conditioned media with anti-bFGF antibody inhibited the regulation of the Nav-D by T3. This suggests that the up-regulation of the neuronal sodium current density by T3 is not a direct effect but involves bFGF release and satellite cells. Thus glial cells can modulate neuronal excitability via secretion of paracrinely acting factors.

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Ligands:   Thyroid hormone





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