A lack of thyroid hormone (T3) in the postnatal period causes an irreversible mental retardation, characterized by a slowing of thoughts and movements accompanied by a characteristic slowing of electroencephalographic parameters. We have previously shown that a lack of T3 down-regulates the voltage-gated sodium- current density (Nav-D) in hippocampal neurons of postnatal rats (Potthoff and Dietzel, 1997), leading to slowed action potential upstrokes and decreased firing frequencies (Hoffmann and Dietzel, 2004). It remained, however, unresolved whether T3 acts directly on neurons or via secondary factors.

Our present investigations show that hippocampal neurons are not directly regulated by T3 but dependent on the presence of glial cells which secrete a heat instable soluble factor to regulate the Nav-D. In the search for the secreted factor we found that bFGF, known to be released from cerebellar glial cells after T3 treatment (Trentin et al. 1997), also increased the Nav-D of hippocampal neurons.

Neutralization assays of astrocyte conditioned media with anti- bFGF inhibited the regulation of the Nav-D by T3. This suggests that bFGF is released from hippocampal astrocytes in response to T3-treatment and up-regulates the Nav-D in neurons.