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

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 depe...

Full description

Saved in:
Bibliographic Details
Published in:Molecular endocrinology (Baltimore, Md.) Md.), 2009-09, Vol.23 (9), p.1494-1504
Main Authors: Niederkinkhaus, Vanessa, Marx, Romy, Hoffmann, Gerd, Dietzel, Irmgard D
Format: Article
Language:English
Subjects:
Animals
Astrocytes - cytology
Fibroblast Growth Factor 2 - metabolism
Hippocampus - metabolism
Models, Biological
Neuroglia - metabolism
Neurons - metabolism
Patch-Clamp Techniques
Rats
Rats, Wistar
Sodium - metabolism
Sodium Channels - metabolism
Triiodothyronine - metabolism
Up-Regulation
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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. Upregulation of neuronal voltage-activated Na+ currents by T3 requires secretion of soluble factors from cocultured satellite cells, is mimicked by bFGF and blocked by anti-bFGF antibodies.
ISSN:0888-8809
1944-9917
DOI:10.1210/me.2009-0132